Related Experiment Video
Updated: Dec 6, 2025

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
Published on: May 14, 2016
Endogenous Anti-Cancer Candidates in GPCR, ER Stress, and EMT
Rohit Gundamaraju1, Wenying Lu2, Iman Azimi3
1ER Stress & Mucosal Immunology Group, School of Health Sciences, University of Tasmania, Launceston, TAS 7248, Australia.
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.
Insights
This review explores how G protein-coupled receptors (GPCRs) and endoplasmic reticulum stress (ER stress) influence cancer. It highlights specific proteins that can trigger apoptosis, offering potential therapeutic strategies for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cellular Signaling
Background:
- Cellular responses to stimuli involve G protein-coupled receptors (GPCRs) and endoplasmic reticulum stress (ER stress).
- GPCR signaling is crucial in many cancers and is a target for numerous clinical drugs.
- Cancer cells often downregulate GPCRs to promote survival, proliferation, and metastasis.
Purpose of the Study:
- To review critical mechanisms where GPCRs and ER stress pathways influence carcinogenesis.
- To identify proteins that can induce apoptosis and serve as therapeutic targets in cancer.
Main Methods:
- Literature review of existing research on GPCRs, ER stress, and cancer.
- Analysis of molecular mechanisms underlying cancer progression and cell survival.
- Identification of pro-apoptotic proteins within these cellular systems.
Main Results:
- GPCRs and ER stress pathways are frequently dysregulated in cancer, often promoting tumor survival and progression.
- Mechanisms like the unfolded protein response (UPR) and epithelial-to-mesenchymal transition (EMT) are implicated in cancer progression.
- Certain proteins within these pathways can paradoxically induce apoptosis, presenting therapeutic opportunities.
Conclusions:
- Understanding the dual role of GPCRs and ER stress in cancer is vital for developing effective treatments.
- Targeting specific pro-apoptotic proteins offers a promising strategy to combat cancer.
- Further research into these mechanisms can pave the way for novel cancer therapies.
More Related Videos
07:43An Enzyme- and Serum-free Neural Stem Cell Culture Model for EMT Investigation Suited for Drug Discovery
Published on: August 23, 2016
07:41A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators
Published on: February 20, 2018
Related Concept Videos
Mitogens and the Cell Cycle
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
G Protein-coupled Receptors
GPCRs are also called heptahelical, 7TM, or serpentine receptors, and consist of seven (H1-H7) transmembrane alpha-helices that span the bilayer to form a cylindrical core. The transmembrane helices are connected by three extracellular loops and three...
The Intrinsic Apoptotic Pathway
GPCRs Regulate Adenylyl Cylase Activity