ArticleCell death discovery2023
GPER deletion triggers inhibitory effects in triple negative breast cancer (TNBC) cells through the JNK/c-Jun/p53/Noxa transduction pathway.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 19 citations in OpenAlex.
- Estradiol Promotes Tumor Progression in ERα-Low Endometrial Cancer via the GPER/SphK1 Pathway.Journal of biochemical and molecular toxicology · 2026Article
- Unraveling the intricate molecular mechanisms of sex hormones' roles in breast cancer pathogenesis: A review.Medicine · 2026Review
- GPER agonist G1 suppresses neuronal apoptosis mediated by endoplasmic reticulum stress after exertional heat stroke injury.Scientific reports · 2026Article
- Endocrine therapy resistance of breast cancer: Important role of G protein-coupled estrogen receptor (GPER) and new therapeutic strategies.Genes & diseases · 2026Review
- More than alternative estrogen receptors: the emerging role of GPER-1 and ERα36 in breast cancer.Exploration of targeted anti-tumor therapy · 2026Review
- Sophoridine inhibits proliferation and migration by targeting PIM1 in breast cancer.Pharmaceutical biology · 2025Article
- Integrin αvβ3 as a Non-Genomic Estrogen Receptor in Breast Cancer for Signaling Pathways and Crosstalk.Cells · 2025Review
- Estrogen Receptors as Key Factors in Carcinogenesis.Biomedicines · 2025Review
- Interactions between LncRNAs and MAPK signaling pathways in the pathogenesis of breast cancer.Cancer cell international · 2025Review
- GPER in metabolic homeostasis and disease: molecular mechanisms, nutritional regulation, and therapeutic potential.Journal of translational medicine · 2025Review
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Interleukin-1β mediates a tumor-supporting environment prompted by IGF1 in triple-negative breast cancer (TNBC).Journal of translational medicine · 2025Article
- CTGF (CCN2): a multifaceted mediator in breast cancer progression and therapeutic targeting.Cancer metastasis reviews · 2025Review
- Interaction of GPER-1 with the endocrine signaling axis in breast cancer.Frontiers in endocrinology · 2025Review
- Whole exome sequencing and bioinformatics reveal PMAIP1 and PDGFRL as immune-related gene markers in follicular thyroid carcinoma.Frontiers in genetics · 2025Article
- Single-cell transcriptomes of dissecting the intra-tumoral heterogeneity of breast cancer microenvironment.Journal of cancer research and clinical oncology · 2024Article
- Differential bone morphology and hypoxia activity in skeletal metastases of ERCommunications biology · 2024Article
- Article
- The G Protein Estrogen Receptor (GPER) is involved in the resistance to the CDK4/6 inhibitor palbociclib in breast cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Estetrol/GPER/SERPINB2 transduction signaling inhibits the motility of triple-negative breast cancer cells.Journal of translational medicine · 2024Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
Abstract
The G protein-coupled estrogen receptor (GPER) mediates estrogen action in different pathophysiological conditions, including cancer. GPER expression and signaling have been found to join in the progression of triple-negative breast cancer (TNBC), even though controversial data have been reported. In present study, we aimed at providing new mechanistic and biological discoveries knocking out (KO) GPER expression by CRISPR/Cas9 technology in MDA-MB-231 TNBC cells. GPER KO whole transcriptome respect to wild type (WT) MDA-MB-231 cells was determined through total RNA sequencing (RNA-Seq) and gene ontology (GO) enrichment analysis. We ascertained that anti-proliferative and pro-apoptotic gene signatures characterize GPER KO MDA-MB-231 cells. Thereafter, we determined that these cells exhibit a reduced proliferative, clonogenic and self-renewal potential along with an increased mitochondria-dependent apoptosis phenotype. In addition, we recognized that decreased cAMP levels trigger the JNK/c-Jun/p53/Noxa axis, which in turn orchestrates the pro-apoptotic effects observed in GPER KO cells. In accordance with these data, survival analyses in TNBC patients of the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) dataset indicated that high Noxa expression correlates with improved outcomes in TNBC patients. Furthermore, we demonstrated that GPER KO in TNBC cells impairs the expression and secretion of the well-acknowledged GPER target gene named CTGF, thus resulting in the inhibition of migratory effects in cancer-associated fibroblasts (CAFs). Overall, the present study provides novel mechanistic and biological insights on GPER KO in TNBC cells suggesting that GPER may be considered as a valuable target in comprehensive therapeutic approaches halting TNBC progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.