Working Paper Review Version 2 This version is not peer-reviewed

Endogenous anti cancer candidates in GPCR, ER stress, and EMT

Version 1 : Received: 5 July 2020 / Approved: 6 July 2020 / Online: 6 July 2020 (08:30:05 CEST)
Version 2 : Received: 8 October 2020 / Approved: 8 October 2020 / Online: 8 October 2020 (13:06:04 CEST)

How to cite: Gundamaraju, R.; Lu, W.; Eri, R. Endogenous anti cancer candidates in GPCR, ER stress, and EMT. Preprints 2020, 2020070097 Gundamaraju, R.; Lu, W.; Eri, R. Endogenous anti cancer candidates in GPCR, ER stress, and EMT. Preprints 2020, 2020070097

Abstract

The majority of cellular responses to external stimuli are mediated by receptors such as G protein-coupled receptors (GPCRs) and systems including endoplasmic reticulum stress (ER stress). Since GPCR signalling is pivotal in numerous malignancies, they are widely targeted by a number of clinical drugs. Cancer cells often negatively modulate GPCRs in order to survive, proliferate and to disseminate. Similarly, numerous branches of the unfolded protein response (UPR) act as pro-survival mediators and are involved in promoting cancer progression via mechanisms such as epithelial to mesenchymal transition (EMT). However, there are a few proteins among these groups which impede deleterious effects by orchestrating the pro-apoptotic phenomenon and paving a therapeutic pathway. The present review exposes and discusses such critical mechanisms and some of the key processes involved in carcinogenesis.

Subject Areas

ER stress; GPCR; EMT; cancer progression; migration; cancer

Comments (1)

Comment 1
Received: 8 October 2020
Commenter: Rohit Gundamaraju
Commenter's Conflict of Interests: Author
Comment: The new updated version has numerous changes including change of title and the content. 
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