Authors :
Priti Dalui; Joydeep Das; Banani Bindhani
Volume/Issue :
Volume 11 - 2026, Issue 3 - March
Google Scholar :
https://tinyurl.com/4v4s9e4p
Scribd :
https://tinyurl.com/4hw3nb8j
DOI :
https://doi.org/10.38124/ijisrt/26mar498
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
Abstract :
Tripple negative breast cancer isthe most aggressive kinds of breast cancer having ER negative, PR negative & HER2
negative leading to limited treatment option. Recentstudiesshowed over expression of G protein – coupled estrogen Receptor
in breast cancer cells. GPER is a membrane bound receptor mediate non-genomic signalling gathered attention for its
complex role. GPER exhibit tumour promoting Properties through GFR – transactivation, PI3K/AKT, MAPK, CAMP,
NFKB pathways leading to cancer. Development, proliferation, metastasis and epithelial mesenchymal transition (EMT).
Likewise, GPER also having tumour suppressive role leading to caspase mediated apoptosis or cell cycle arrest in G2/M
phase. GPER also inhibit proliferation, suppress EMT & reduce migratory potential suggesting a protective role against
metastasis. Certain selective drugs of breast cancer like tamoxifen show resistance in GPER activated TNBC cells which
cause GPER to be a potential target against breast cancer. This review explores along with mote dual role of GPER in TNBC,
along with molecular mechanism & clinical approach of targeting GPER for therapeutic strategy challenging breast cancer
subtypes.
Keywords :
Tripple Negative Breast Cancer (TNBC), G-Protein Coupled Estrogen Receptor (GPER), PI3K/AKT, MAPK, CAMP, NFKB, Epithelial Mesenchymal Transition (EMT).
References :
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Tripple negative breast cancer isthe most aggressive kinds of breast cancer having ER negative, PR negative & HER2
negative leading to limited treatment option. Recentstudiesshowed over expression of G protein – coupled estrogen Receptor
in breast cancer cells. GPER is a membrane bound receptor mediate non-genomic signalling gathered attention for its
complex role. GPER exhibit tumour promoting Properties through GFR – transactivation, PI3K/AKT, MAPK, CAMP,
NFKB pathways leading to cancer. Development, proliferation, metastasis and epithelial mesenchymal transition (EMT).
Likewise, GPER also having tumour suppressive role leading to caspase mediated apoptosis or cell cycle arrest in G2/M
phase. GPER also inhibit proliferation, suppress EMT & reduce migratory potential suggesting a protective role against
metastasis. Certain selective drugs of breast cancer like tamoxifen show resistance in GPER activated TNBC cells which
cause GPER to be a potential target against breast cancer. This review explores along with mote dual role of GPER in TNBC,
along with molecular mechanism & clinical approach of targeting GPER for therapeutic strategy challenging breast cancer
subtypes.
Keywords :
Tripple Negative Breast Cancer (TNBC), G-Protein Coupled Estrogen Receptor (GPER), PI3K/AKT, MAPK, CAMP, NFKB, Epithelial Mesenchymal Transition (EMT).