1
40
9
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3390/nu9050436" target="_blank" rel="noreferrer noopener">http://doi.org/10.3390/nu9050436</a>
Issue
5
Volume
9
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Anti-Inflammatory Mechanism Involved in Pomegranate-Mediated Prevention of Breast Cancer: the Role of NF-kappaB and Nrf2 Signaling Pathways.
Publisher
An entity responsible for making the resource available
Nutrients
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-04
Subject
The topic of the resource
Female; Animals; Anti-Inflammatory Agents/*pharmacology; Rats; Gene Expression Regulation; Signal Transduction; Apoptosis/drug effects; anti-inflammatory effects; Anticarcinogenic Agents/pharmacology; breast tumor; COX-2; Cyclooxygenase 2/genetics/metabolism; DMBA; HSP90; HSP90 Heat-Shock Proteins/genetics/metabolism; I-kappa B Kinase/genetics/metabolism; NF-E2-Related Factor 2/genetics/*metabolism; NF-kappa B/genetics/*metabolism; NF-kappaB; Nrf2; Plant Preparations/*pharmacology; Punica granatum; Punicaceae/*chemistry; Pomegranate; Chemoprevention; Dose-Response Relationship; Drug; Neoplastic; Mammary Neoplasms; 10-Dimethyl-1; 9; Neoplastic/drug effects; Cell Transformation; 2-benzanthracene/toxicity; Experimental/*prevention & control; Animal Studies; Breast Neoplasms; Inflammation Mediators; Physical Education and Training; Neoplasms – Prevention and Control
Creator
An entity primarily responsible for making the resource
Mandal Animesh; Bhatia Deepak; Bishayee Anupam
Description
An account of the resource
Pomegranate (Punica granatum L.), a nutrient-rich unique fruit, has been used for centuries for the prevention and treatment of various inflammation-driven diseases. Based on our previous study, a characterized pomegranate emulsion (PE) exhibited a striking inhibition of dimethylbenz(a)anthracene (DMBA)-initiated rat mammary tumorigenesis via antiproliferative and apoptosis-inducing mechanisms. The objective of the present work is to investigate the anti-inflammatory mechanism of action of PE during DMBA rat mammary carcinogenesis by evaluating the expression of cyclooxygenase-2 (COX-2), heat shock protein 90 (HSP90), nuclear factor-kappaB (NF-kappaB) and nuclear factor erythroid 2p45 (NF-E2)-related factor 2 (Nrf2). Mammary tumor samples were harvested from our previous chemopreventive study in which PE (0.2-5.0 g/kg) was found to reduce mammary tumorigenesis in a dose-dependent manner. The expressions of COX-2, HSP90, NF-kappaB, inhibitory kappaBalpha (IkappaBalpha) and Nrf2 were detected by immunohistochemical techniques. PE decreased the expression of COX-2 and HSP90, prevented the degradation of IkappaBalpha, hindered the translocation of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3390/nu9050436" target="_blank" rel="noreferrer noopener">10.3390/nu9050436</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
10-Dimethyl-1
2-benzanthracene/toxicity
2017
9
Animal Studies
Animals
Anti-Inflammatory Agents/*pharmacology
anti-inflammatory effects
Anticarcinogenic Agents/pharmacology
Apoptosis/drug effects
Bhatia Deepak
Bishayee Anupam
Breast Neoplasms
breast tumor
Cell Transformation
Chemoprevention
COX-2
Cyclooxygenase 2/genetics/metabolism
DMBA
Dose-Response Relationship
Drug
Experimental/*prevention & control
Female
Gene Expression Regulation
HSP90
HSP90 Heat-Shock Proteins/genetics/metabolism
I-kappa B Kinase/genetics/metabolism
Inflammation Mediators
Mammary Neoplasms
Mandal Animesh
Neoplasms – Prevention and Control
Neoplastic
Neoplastic/drug effects
NF-E2-Related Factor 2/genetics/*metabolism
NF-kappa B/genetics/*metabolism
NF-kappaB
Nrf2
Nutrients
Physical Education and Training
Plant Preparations/*pharmacology
Pomegranate
Punica granatum
Punicaceae/*chemistry
Rats
Signal Transduction
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.18632/oncotarget.4430" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.4430</a>
Pages
16757–16765
Issue
18
Volume
6
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Six stroma-based RNA markers diagnostic for prostate cancer in European-Americans validated at the RNA and protein levels in patients in China.
Publisher
An entity responsible for making the resource available
Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-06
Subject
The topic of the resource
diagnosis; Adult; Humans; prostate cancer; Male; Middle Aged; Aged; Young Adult; Gene Expression Profiling; Gene Expression Regulation; Tumor Microenvironment; Biomarkers; China; European Continental Ancestry Group/genetics; microenvironment; Prostate/pathology; Prostatic Neoplasms/*diagnosis/*genetics; race; stroma; 80 and over; Neoplastic; Tumor/*genetics
Creator
An entity primarily responsible for making the resource
Zhu Jian-Guo; Pan Cong; Jiang Jun; Deng Mingsen; Gao Hengjun; Men Bozhao; McClelland Michael; Mercola Dan; Zhong Wei-D; Jia Zhenyu
Description
An account of the resource
We previously analyzed human prostate tissue containing stroma near to tumor and from cancer-negative tissues of volunteers. Over 100 candidate gene expression differences were identified and used to develop a classifier that could detect nearby tumor with an accuracy of 97% (sensitivity = 98% and specificity = 88%) based on 364 independent test cases from primarily European American cases. These stroma-based gene signatures have the potential to identify cancer patients among those with negative biopsies. In this study, we used prostate tissues from Chinese cases to validate six of these markers (CAV1, COL4A2, HSPB1, ITGB3, MAP1A and MCAM). In validation by real-time PCR, four genes (COL4A2, HSPB1, ITGB3, and MAP1A) demonstrated significantly lower expression in tumor-adjacent stroma compared to normal stroma (p value
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.4430" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.4430</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
80 and over
Adult
Aged
Biomarkers
China
Deng Mingsen
Diagnosis
European Continental Ancestry Group/genetics
Gao Hengjun
Gene Expression Profiling
Gene Expression Regulation
Humans
Jia Zhenyu
Jiang Jun
Male
McClelland Michael
Men Bozhao
Mercola Dan
microenvironment
Middle Aged
Neoplastic
Oncotarget
Pan Cong
Prostate cancer
Prostate/pathology
Prostatic Neoplasms/*diagnosis/*genetics
Race
stroma
Tumor Microenvironment
Tumor/*genetics
Young Adult
Zhong Wei-D
Zhu Jian-Guo
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.18632/oncotarget.2676" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.2676</a>
Pages
1286–1301
Issue
2
Volume
6
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A class of genes in the HER2 regulon that is poised for transcription in breast cancer cell lines and expressed in human breast tumors.
Publisher
An entity responsible for making the resource available
Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-01
Subject
The topic of the resource
Humans; Cell Line; *Gene Expression Regulation; Reverse Transcriptase Polymerase Chain Reaction; *Gene Expression Profiling; Breast Neoplasms/genetics/pathology; Gene Regulatory Networks; Homeodomain Proteins/genetics/metabolism; MCF-7 Cells; Nanog Homeobox Protein; Neoplastic Stem Cells/metabolism; Octamer Transcription Factor-3/genetics/metabolism; Regulon/*genetics; RNA Polymerase II/metabolism; SOXB1 Transcription Factors/genetics/metabolism; Tumor Microenvironment/genetics; Receptor; Blotting; Western; Tumor; Neoplastic; ErbB-2/*genetics/metabolism
Creator
An entity primarily responsible for making the resource
Rahmatpanah Farah B; Jia Zhenyu; Chen Xin; Char Jessica E; Men Bozhao; Franke Anna-Clara; Jones Frank E; McClelland Michael; Mercola Dan
Description
An account of the resource
HER2-positive breast cancer accounts for 25% of all cases and has a poor prognosis. Although progress has been made in understanding signal transduction, little is known of how HER2 achieves gene regulation. We performed whole genome expression analysis on a HER2(+) and HER2(-) breast cancer cell lines and compared these results to expression in 812 primary tumors stratified by their HER2 expression level. Chip-on-chip with anti-RNA polymerase II was compared among breast cancer cell lines to identify genes that are potentially activated by HER2. The expression levels of these HER2-dependent POL II binding genes were determined for the 812 HER2+/- breast cancer tissues. Genes differentially expressed between HER2+/- cell lines were generally regulated in the same direction as in breast cancer tissues. We identified genes that had POLII binding in HER2(+) cell lines, but without significant gene expression. Of 737 such genes "poised" for expression in cell lines, 113 genes were significantly differentially expressed in breast tumors in a HER2-dependent manner. Pathway analysis of these 113 genes revealed that a large group of genes were associated with stem cell and progenitor cell control as indicated by networks centered on NANOG, SOX2, OCT3/4. HER2 directs POL II binding to a large number of genes in breast cancer cells. A "poised" class of genes in HER2(+) cell lines with POLII binding and low RNA expression but is differentially expressed in primary tumors, strongly suggests a role of the microenvironment and further suggests a role for stem cells proliferation in HER2-regulated breast cancer tissue.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.2676" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.2676</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Profiling
*Gene Expression Regulation
2015
Blotting
Breast Neoplasms/genetics/pathology
Cell Line
Char Jessica E
Chen Xin
ErbB-2/*genetics/metabolism
Franke Anna-Clara
Gene Regulatory Networks
Homeodomain Proteins/genetics/metabolism
Humans
Jia Zhenyu
Jones Frank E
McClelland Michael
MCF-7 Cells
Men Bozhao
Mercola Dan
Nanog Homeobox Protein
Neoplastic
Neoplastic Stem Cells/metabolism
Octamer Transcription Factor-3/genetics/metabolism
Oncotarget
Rahmatpanah Farah B
Receptor
Regulon/*genetics
Reverse Transcriptase Polymerase Chain Reaction
RNA Polymerase II/metabolism
SOXB1 Transcription Factors/genetics/metabolism
Tumor
Tumor Microenvironment/genetics
Western
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1371/journal.pone.0115919" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0115919</a>
Pages
e0115919–e0115919
Issue
1
Volume
10
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
MiR-21 enhances melanoma invasiveness via inhibition of tissue inhibitor of metalloproteinases 3 expression: in vivo effects of MiR-21 inhibitor.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015
Subject
The topic of the resource
Humans; Gene Expression Regulation; Cell Line; MicroRNAs/*genetics/metabolism; Cell Movement/genetics; Cell Proliferation/genetics; Melanoma/*genetics/metabolism/pathology; Neoplasm Invasiveness/*genetics/pathology; Skin Neoplasms/*genetics/metabolism/pathology; Tissue Inhibitor of Metalloproteinase-3/*genetics/metabolism; RNA; Tumor; Neoplastic; Small Interfering
Creator
An entity primarily responsible for making the resource
Martin del Campo Sara E; Latchana Nicholas; Levine Kala M; Grignol Valerie P; Fairchild Ene T; Jaime-Ramirez Alena Cristina; Dao Thao-Vi; Karpa Volodymyr I; Carson Mary; Ganju Akaansha; Chan Anthony N; Carson William E 3rd
Description
An account of the resource
Metastatic melanoma is the most aggressive form of this cancer. It is important to understand factors that increase or decrease metastatic activity in order to more effectively research and implement treatments for melanoma. Increased cell invasion through the extracellular matrix is required for metastasis and is enhanced by matrix metalloproteinases (MMPs). Tissue inhibitor of metalloproteinases 3 (TIMP3) inhibits MMP activity. It was previously shown by our group that miR-21, a potential regulator of TIMP3, is over-expressed in cutaneous melanoma. It was therefore hypothesized that increased levels of miR-21 expression would lead to decreased expression of TIMP3 and thereby enhance the invasiveness of melanoma cells. miR-21 over-expression in the melanoma cell lines WM1552c, WM793b, A375 and MEL 39 was accomplished via transfection with pre-miR-21. Immunoblot analysis of miR-21-overexpressing cell lines revealed reduced expression of TIMP3 as compared to controls. This in turn led to a significant increase in the invasiveness of the radial growth phase cell line WM1552c and the vertical growth phase cell line WM793b (p \textless 0.05), but not in the metastatic cell lines A375 or MEL 39. The proliferation and migration of miR-21 over-expressing cell lines was not affected. Reduced expression of TIMP3 was achieved by siRNA knockdown and significantly enhanced invasion of melanoma cell lines, mimicking the effects of miR-21 over-expression. Treatment of tumor cells with a linked nucleic acid antagomir to miR-21 inhibited tumor growth and increased tumor expression of TIMP3 in vivo in 01B74 Athymic NCr-nu/nu mice. Intra-tumoral injections of anti-miR-21 produced similar effects. This data shows that increased expression of miR-21 enhanced the invasive potential of melanoma cell lines through TIMP3 inhibition. Therefore, inhibition of miR-21 in melanoma may reduce melanoma invasiveness.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0115919" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0115919</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Carson Mary
Carson William E 3rd
Cell Line
Cell Movement/genetics
Cell Proliferation/genetics
Chan Anthony N
Dao Thao-Vi
Fairchild Ene T
Ganju Akaansha
Gene Expression Regulation
Grignol Valerie P
Humans
Jaime-Ramirez Alena Cristina
Karpa Volodymyr I
Latchana Nicholas
Levine Kala M
Martin del Campo Sara E
Melanoma/*genetics/metabolism/pathology
MicroRNAs/*genetics/metabolism
Neoplasm Invasiveness/*genetics/pathology
Neoplastic
PloS one
RNA
Skin Neoplasms/*genetics/metabolism/pathology
Small Interfering
Tissue Inhibitor of Metalloproteinase-3/*genetics/metabolism
Tumor
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1155/2014/746979" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2014/746979</a>
Pages
746979–746979
Volume
2014
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Establishing reliable miRNA-cancer association network based on text-mining method.
Publisher
An entity responsible for making the resource available
Computational and mathematical methods in medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
1905-7
Subject
The topic of the resource
Algorithms; Area Under Curve; Computational Biology/*methods; Data Mining/*methods; False Positive Reactions; Gene Expression Profiling/methods; Gene Expression Regulation; Gene Regulatory Networks; Humans; MicroRNAs/*genetics/*metabolism; Neoplasms/*genetics/metabolism; Neoplastic; Probability; Reproducibility of Results
Creator
An entity primarily responsible for making the resource
Li Lun; Hu Xingchi; Yang Zhaowan; Jia Zhenyu; Fang Ming; Zhang Libin; Zhou Yanhong
Description
An account of the resource
Associating microRNAs (miRNAs) with cancers is an important step of understanding the mechanisms of cancer pathogenesis and finding novel biomarkers for cancer therapies. In this study, we constructed a miRNA-cancer association network (miCancerna) based on more than 1,000 miRNA-cancer associations detected from millions of abstracts with the text-mining method, including 226 miRNA families and 20 common cancers. We further prioritized cancer-related miRNAs at the network level with the random-walk algorithm, achieving a relatively higher performance than previous miRNA disease networks. Finally, we examined the top 5 candidate miRNAs for each kind of cancer and found that 71% of them are confirmed experimentally. miCancerna would be an alternative resource for the cancer-related miRNA identification.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2014/746979" target="_blank" rel="noreferrer noopener">10.1155/2014/746979</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Algorithms
Area Under Curve
Computational and mathematical methods in medicine
Computational Biology/*methods
Data Mining/*methods
False Positive Reactions
Fang Ming
Gene Expression Profiling/methods
Gene Expression Regulation
Gene Regulatory Networks
Hu Xingchi
Humans
Jia Zhenyu
Li Lun
MicroRNAs/*genetics/*metabolism
Neoplasms/*genetics/metabolism
Neoplastic
Probability
Reproducibility of Results
Yang Zhaowan
Zhang Libin
Zhou Yanhong
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.suronc.2016.05.017" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.suronc.2016.05.017</a>
Pages
184–189
Issue
3
Volume
25
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
MicroRNA dysregulation in melanoma.
Publisher
An entity responsible for making the resource available
Surgical oncology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
*Gene Expression Regulation; *Melanoma; *MicroRNA; Disease Progression; Humans; Melanoma/*genetics/*pathology; MicroRNAs/*genetics; Neoplastic; Prognosis
Creator
An entity primarily responsible for making the resource
Latchana Nicholas; Ganju Akaansha; Howard J Harrison; Carson William E 3rd
Description
An account of the resource
Melanoma is the deadliest form of skin cancer. Current challenges facing the management of melanoma include accurate prediction of individuals who will respond to adjuvant therapies as well as early detection of recurrences. These and other challenges have prompted investigation into biomarkers that could be used as diagnostic, prognostic and therapeutic aids. MicroRNAs (miRs) are small
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.suronc.2016.05.017" target="_blank" rel="noreferrer noopener">10.1016/j.suronc.2016.05.017</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
*Melanoma
*MicroRNA
2016
Carson William E 3rd
Disease Progression
Ganju Akaansha
Howard J Harrison
Humans
Latchana Nicholas
Melanoma/*genetics/*pathology
MicroRNAs/*genetics
Neoplastic
Prognosis
Surgical oncology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.canlet.2016.05.014</a>
Pages
131–141
Issue
2
Volume
378
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Lipopolysaccharide supports maintaining the stemness of CD133(+) hepatoma cells through activation of the NF-kappaB/HIF-1alpha pathway.
Publisher
An entity responsible for making the resource available
Cancer letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-08
Subject
The topic of the resource
*Cancer stem cells; *Lipopolysaccharide; *Plasticity; *Stemness maintenance; *Tumor microenvironment; AC133 Antigen/genetics/*metabolism; alpha Subunit/genetics/*metabolism; Animals; Antineoplastic Agents – Pharmacodynamics; Antineoplastic Agents/pharmacology; Body Weights and Measures; Carcinoma; Cell Line; Cell Movement – Drug Effects; Cell Movement/drug effects; Cell Physiology; Cell Physiology – Drug Effects; Cell Proliferation/drug effects; Drug Resistance; Gene Expression Regulation; Genes; Genetic Techniques; Hepatocellular; Hepatocellular – Drug Therapy; Hepatocellular – Metabolism; Hepatocellular – Pathology; Hepatocellular/drug therapy/genetics/*metabolism/pathology; Humans; Hypoxia-Inducible Factor 1; Inbred BALB C; Lipopolysaccharides – Pharmacodynamics; Lipopolysaccharides/*pharmacology; Liver Neoplasms; Liver Neoplasms – Drug Therapy; Liver Neoplasms – Metabolism; Liver Neoplasms – Pathology; Liver Neoplasms/drug therapy/genetics/*metabolism/pathology; Male; Mice; Neoplasm; Neoplasm Invasiveness; Neoplastic; Neoplastic Stem Cells/*drug effects/metabolism/pathology; NF-kappa B – Metabolism; NF-kappa B/*metabolism; Nude; Phenotype; Proteins; Proteins – Metabolism; RNA Interference; Signal Transduction – Drug Effects; Signal Transduction/drug effects; Stem Cells – Drug Effects; Stem Cells – Metabolism; Stem Cells – Pathology; Time Factors; Transfection; Tumor Burden; Tumor Microenvironment
Creator
An entity primarily responsible for making the resource
Lai Fo-Bao; Liu Wen-Ting; Jing Ying-Ying; Yu Guo-Feng; Han Zhi-Peng; Yang Xue; Zeng Jian-Xing; Zhang Hang-Jie; Shi Rong-Yu; Li Xiao-Yong; Pan Xiao-Rong; Li Rong; Zhao Qiu-Dong; Wu Meng-Chao; Zhang Ping; Liu Jing-Feng; Wei Li-Xin
Description
An account of the resource
Due to the existence of cancer stem cells (CSCs), persistence and relapse of human hepatocellular carcinoma (HCC) are common after treatment with existing anti-cancer therapies. Emerging evidence indicates that lipopolysaccharide (LPS) plays a crucial role in aggravating HCC, but information about the effect of LPS on CSCs of HCC remains scant. Here, we report that the stemness of CD133(+) CSCs sorted from the human HCC cell line Huh7 was maintained well when cells were cultured with LPS. The reduction of CD133 expression was much lesser in cultured CSCs in the presence of LPS. In response to LPS stimulation, CSCs showed an increase in their activity of clonogenesis and tumorigenesis. LPS also supported maintaining CSC abilities of migration, invasion, and chemo-resistance. Treatment with HIF-1alpha-specific siRNA significantly reduced CD133 expression by CSCs at both mRNA and protein levels. Further, the expression of HIF-1alpha and CD133 was reduced in LPS-stimulated CSCs when the NF-kappaB inhibitor was added to the cell culture. HIF-1alpha-specific siRNA also effectively counteracted the effect of LPS on maintaining CSC abilities of migration and invasion. These data indicate that LPS, an important mediator in the liver tumor microenvironment, supports the maintenance of CSC stemness through signaling of the NF-kappaB/HIF-1alpha pathway. Our current study highlights LPS as a potential target for developing new therapeutic approaches to eliminate CSCs during the treatment of HCC.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">10.1016/j.canlet.2016.05.014</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cancer stem cells
*Lipopolysaccharide
*Plasticity
*Stemness maintenance
*Tumor microenvironment
2016
AC133 Antigen/genetics/*metabolism
alpha Subunit/genetics/*metabolism
Animals
Antineoplastic Agents – Pharmacodynamics
Antineoplastic Agents/pharmacology
Body Weights and Measures
Cancer letters
Carcinoma
Cell Line
Cell Movement – Drug Effects
Cell Movement/drug effects
Cell Physiology
Cell Physiology – Drug Effects
Cell Proliferation/drug effects
Department of Integrative Medical Sciences
Drug Resistance
Gene Expression Regulation
Genes
Genetic Techniques
Han Zhi-Peng
Hepatocellular
Hepatocellular – Drug Therapy
Hepatocellular – Metabolism
Hepatocellular – Pathology
Hepatocellular/drug therapy/genetics/*metabolism/pathology
Humans
Hypoxia-Inducible Factor 1
Inbred BALB C
Jing Ying-Ying
Lai Fo-Bao
Li Rong
Li Xiao-Yong
Lipopolysaccharides – Pharmacodynamics
Lipopolysaccharides/*pharmacology
Liu Jing-Feng
Liu Wen-Ting
Liver Neoplasms
Liver Neoplasms – Drug Therapy
Liver Neoplasms – Metabolism
Liver Neoplasms – Pathology
Liver Neoplasms/drug therapy/genetics/*metabolism/pathology
Male
Mice
NEOMED College of Medicine
Neoplasm
Neoplasm Invasiveness
Neoplastic
Neoplastic Stem Cells/*drug effects/metabolism/pathology
NF-kappa B – Metabolism
NF-kappa B/*metabolism
Nude
Pan Xiao-Rong
Phenotype
Proteins
Proteins – Metabolism
RNA Interference
Shi Rong-Yu
Signal Transduction – Drug Effects
Signal Transduction/drug effects
Stem Cells – Drug Effects
Stem Cells – Metabolism
Stem Cells – Pathology
Time Factors
Transfection
Tumor Burden
Tumor Microenvironment
Wei Li-Xin
Wu Meng-Chao
Yang Xue
Yu Guo-Feng
Zeng Jian-Xing
Zhang Hang-Jie
Zhang Ping
Zhao Qiu-Dong
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/jcp.25900" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcp.25900</a>
Pages
409–421
Issue
1
Volume
233
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Osteoactivin regulates head and neck squamous cell carcinoma invasion by modulating matrix metalloproteases.
Publisher
An entity responsible for making the resource available
Journal of cellular physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
*Cell Movement; Carcinoma; Cell Line; cell lines; Enzymologic; extracellular matrix; Gene Expression Regulation; Head and Neck Neoplasms/*enzymology/genetics/pathology; human; Humans; matrix metalloproteinases; Matrix Metalloproteinases; Membrane Glycoproteins/genetics/*metabolism; Messenger/genetics/metabolism; neoplasm invasion; Neoplasm Invasiveness; Neoplastic; RNA; RNA Interference; Secreted/genetics/*metabolism; Signal Transduction; Squamous Cell Carcinoma of Head and Neck; Squamous Cell/*enzymology/genetics/pathology; Transfection; Tumor
Creator
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Arosarena Oneida A; Barr Eric W; Thorpe Ryan; Yankey Hilary; Tarr Joseph T; Safadi Fayez F
Description
An account of the resource
Nearly 60% of patients with head and neck squamous cell carcinoma (HNSCC) die of metastases or locoregional recurrence. Metastasis is mediated by cancer cell migration and invasion, which are in part dependent on extracellular matrix degradation by matrix metalloproteinases. Osteoactivin (OA) overexpression plays a role in metastases in several malignancies, and has been shown to upregulate matrix metalloproteinase (MMP) expression and activity. To determine how OA modulates MMP expression and activity in HNSCC, and to investigate OA effects on cell invasion, we assessed effects of OA treatment on MMP mRNA and protein expression, as well as gelatinase and caseinolytic activity in HNSCC cell lines. We assessed the effects of OA gene silencing on MMP expression, gelatinase and caseinolytic activity, and cell invasion. OA treatment had differential effects on MMP mRNA expression. OA treatment upregulated MMP-10 expression in UMSCC14a (p = 0.0431) and SCC15 (p \textless 0.0001) cells, but decreased MMP-9 expression in UMSCC14a cells (p = 0.0002). OA gene silencing decreased MMP-10 expression in UMSCC12 cells (p = 0.0001), and MMP-3 (p = 0.0005) and -9 (p = 0.0036) expression in SCC25 cells. In SCC15 and SCC25 cells, OA treatment increased MMP-2 (p = 0.0408) and MMP-9 gelatinase activity (p \textless 0.0001), respectively. OA depletion decreased MMP-2 (p = 0.0023) and -9 (p \textless 0.0001) activity in SCC25 cells. OA treatment increased 70 kDa caseinolytic activity in UMSCC12 cells consistent with tissue type plasminogen activator (p = 0.0078). OA depletion decreased invasive capacity of UMSCC12 cells (p \textless 0.0001). OA's effects on MMP expression in HNSCC are variable, and may promote cancer cell invasion.
Identifier
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<a href="http://doi.org/10.1002/jcp.25900" target="_blank" rel="noreferrer noopener">10.1002/jcp.25900</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cell Movement
2018
Arosarena Oneida A
Barr Eric W
Carcinoma
Cell Line
cell lines
Department of Anatomy & Neurobiology
Enzymologic
Extracellular Matrix
Gene Expression Regulation
Head and Neck Neoplasms/*enzymology/genetics/pathology
Human
Humans
Journal of cellular physiology
matrix metalloproteinases
Membrane Glycoproteins/genetics/*metabolism
Messenger/genetics/metabolism
NEOMED College of Medicine
neoplasm invasion
Neoplasm Invasiveness
Neoplastic
RNA
RNA Interference
Safadi Fayez F
Secreted/genetics/*metabolism
Signal Transduction
Squamous Cell Carcinoma of Head and Neck
Squamous Cell/*enzymology/genetics/pathology
Tarr Joseph T
Thorpe Ryan
Transfection
Tumor
Yankey Hilary
-
Text
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URL Address
<a href="http://doi.org/10.1002/jcp.25279" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcp.25279</a>
Pages
1761–1770
Issue
8
Volume
231
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Osteoactivin Promotes Migration of Oral Squamous Cell Carcinomas.
Publisher
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Journal of cellular physiology
Date
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2016
2016-08
Subject
The topic of the resource
*Cell Movement; Carcinoma; Cell Adhesion; Cell Line; Cell Proliferation; Cell Survival; Enzyme Activation; Gene Expression Regulation; Head and Neck Neoplasms/genetics/*metabolism/pathology; Humans; Integrin beta1/metabolism; Membrane Glycoproteins/genetics/*metabolism; Messenger/metabolism; Mitogen-Activated Protein Kinases/metabolism; Mouth Neoplasms/genetics/*metabolism/pathology; Neoplasm Invasiveness; Neoplastic; Protein Binding; RNA; RNA Interference; Signal Transduction; Squamous Cell Carcinoma of Head and Neck; Squamous Cell/genetics/*metabolism/pathology; Time Factors; Transfection; Tumor
Creator
An entity primarily responsible for making the resource
Arosarena Oneida A; Dela Cadena Raul A; Denny Michael F; Bryant Evan; Barr Eric W; Thorpe Ryan; Safadi Fayez F
Description
An account of the resource
Nearly 50% of patients with oral squamous cell carcinoma (OSCC) die of metastases or locoregional recurrence. Metastasis is mediated by cancer cell adhesion, migration, and invasion. Osteoactivin (OA) overexpression plays a role in metastases in several malignancies. The aims were to determine how integrin interactions modulate OA-induced OSCC cell migration; and to investigate OA effects on cell survival and proliferation. We confirmed OA mRNA and protein overexpression in OSCC cell lines. We assessed OA's interactions with integrins using adhesion inhibition assays, fluorescent immunocytochemistry and co-immunoprecipitation. We investigated OA-mediated activation of mitogen-activated protein kinases (MAPKs) and cell survival. Integrin inhibition effects on OA-mediated cell migration were determined. We assessed effects of OA knock-down on cell migration and proliferation. OA is overexpressed in OSCC cell lines, and serves as a migration-promoting adhesion molecule. OA co-localized with integrin subunits, and co-immunoprecipitated with the subunits. Integrin blocking antibodies, especially those directed against the beta1 subunit, inhibited cell adhesion (P = 0.03 for SCC15 cells). Adhesion to OA activated MAPKs in UMSCC14a cells and OA treatment promoted survival of SCC15 cells. Integrin-neutralizing antibodies enhanced cell migration with OA in the extracellular matrix. OA knock-down resulted in decreased proliferation of SCC15 and SCC25 cells, but did not inhibit cell migration. OA in the extracellular matrix promotes OSCC cell adhesion and migration, and may be a novel target in the prevention of HNSCC spread. J. Cell. Physiol. 231: 1761-1770, 2016. (c) 2015 Wiley Periodicals, Inc.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/jcp.25279" target="_blank" rel="noreferrer noopener">10.1002/jcp.25279</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cell Movement
2016
Arosarena Oneida A
Barr Eric W
Bryant Evan
Carcinoma
Cell Adhesion
Cell Line
Cell Proliferation
Cell Survival
Dela Cadena Raul A
Denny Michael F
Department of Anatomy & Neurobiology
Enzyme Activation
Gene Expression Regulation
Head and Neck Neoplasms/genetics/*metabolism/pathology
Humans
Integrin beta1/metabolism
Journal of cellular physiology
Membrane Glycoproteins/genetics/*metabolism
Messenger/metabolism
Mitogen-Activated Protein Kinases/metabolism
Mouth Neoplasms/genetics/*metabolism/pathology
NEOMED College of Medicine
Neoplasm Invasiveness
Neoplastic
Protein Binding
RNA
RNA Interference
Safadi Fayez F
Signal Transduction
Squamous Cell Carcinoma of Head and Neck
Squamous Cell/genetics/*metabolism/pathology
Thorpe Ryan
Time Factors
Transfection
Tumor