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The Dual Role of GPER in Triple-Negative Breast Cancer: Divergent Modulator of Tumor Progression and Suppression


Authors : Priti Dalui; Joydeep Das; Banani Bindhani

Volume/Issue : Volume 11 - 2026, Issue 3 - March


Google Scholar : https://tinyurl.com/4v4s9e4p

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DOI : https://doi.org/10.38124/ijisrt/26mar498

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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).

Paper Submission Last Date
31 - March - 2026

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