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<a href="http://doi.org/10.1002/jcb.29326" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcb.29326</a>
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Title
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N-end rule pathway inhibitor sensitizes cancer cells to antineoplastic agents by regulating XIAP and RAD21 protein expression
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Journal of Cellular Biochemistry
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2019
2019-08
Subject
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apoptosis; Biochemistry & Molecular Biology; cancer; Cell Biology; cleavage; cyclin; degradation; drug sensitivity; hdm2; heterovalent inhibitors; mechanisms; N-end rule; oncoprotein; RAD21; reaper; substrate; UBR1; XIAP
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Pore Subrata K; Ganguly Anirban; Sau Samaresh; Godeshala Sudhakar; Kanugula Anantha K; Ummanni Ramesh; Kotamraju Srigiridhar; Banerjee Rajkumar
Description
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Anticancer drugs exert their effects on cancer cells by deregulating many pathways linked to cell cycle, apoptosis, etc. but cancer cells gradually become resistive against anticancer drugs, thereby necessitating the development of newer generation anticancer molecules. N-end rule pathway has been shown to be involved in the degradation of many cell cycle and apoptosis-related proteins. However, the involvements of this pathway in cancer are not well established. Recently, we developed a non-peptide-based N-end rule pathway inhibitor, RF-C11 for type 1 and 2 recognition domains of E3 ubiquitin ligases. The inhibitor significantly increased the half-life of potential N-degrons leading to significant physiological changes in vivo. We hypothesized RF-C11 may be used to decipher the N-end rule pathway's role in cancer towards the development of anticancer therapeutics. In this study, we showed that RF-C11, barring noncancer cells, significantly sensitizes cancer cells towards different anticancer agents tested. We further find that the profound cellular sensitization to anticancer drugs was affected by (a) downregulation of X-linked inhibitor of apoptosis protein, an antiapoptotic protein and (b) by stabilization of RAD21, and thereby inhibiting metaphase to anaphase promotion. The study shows that RF-C11 or its analogs may be used as a novel additive in combination therapy against cancer.
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<a href="http://doi.org/10.1002/jcb.29326" target="_blank" rel="noreferrer noopener">10.1002/jcb.29326</a>
2019
Apoptosis
Banerjee Rajkumar
Biochemistry & Molecular Biology
Cancer
Cell Biology
cleavage
cyclin
degradation
Department of Integrative Medical Sciences
drug sensitivity
Ganguly Anirban
Godeshala Sudhakar
hdm2
heterovalent inhibitors
Journal of cellular biochemistry
Kanugula Anantha K
Kotamraju Srigiridhar
mechanisms
N-end rule
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
oncoprotein
Pore Subrata K
RAD21
reaper
Sau Samaresh
September 2019 Update
substrate
UBR1
Ummanni Ramesh
XIAP