ArticleCell death & disease2022
GNG2 acts as a tumor suppressor in breast cancer through stimulating MRAS signaling.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Uncovering Oncogenic Mechanisms of Tumor Suppressor Genes in Breast Cancer Multi-Omics Data.International journal of molecular sciences · 2022Pooled it
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- Identification of susceptibility modules and genes through WGCNA and ceRNA network analysis in neuropathic pain-induced anxiodepression.Translational psychiatry · 2026Article
- OTUD4 deubiquitination stabilizes EGFR and activates the PI3K/AKT pathway to promote the invasiveness of triple-negative breast cancer.Cell death & disease · 2026Article
- Astragaloside IV Ameliorates Diabetic Cardiomyopathy by Suppressing the GNG2/MRAS-ERK Signaling Pathway.International journal of general medicine · 2026Article
- Decitabine Induces Subtype-Specific Epigenomic Remodeling and Perturbs Age-Associated Regulatory CpGs in Breast Cancer.Cancer informatics · 2026Article
- Knockdown of HGH1 in breast cancer cell lines can inhibit the viability, invasion and migration of tumor cells.Cell adhesion & migration · 2025Article
- Independent validation of lung adenocarcinoma prognostic risk scores incorporating cholesterol and estrogen metabolism related transcriptional biomarkers.Scientific reports · 2025Article
- Identification and Verification of Potential Markers Related to Myocardial Fibrosis by Bioinformatics Analysis.Biochemical genetics · 2025Review
- Investigating the effects of miR-526b and miR-655 on doxorubicin sensitivity in breast cancer.Scientific reports · 2025Article
- GNG2 inhibits brain metastases from colorectal cancer via PI3K/AKT/mTOR signaling pathway.Scientific reports · 2025Article
- Dual PI3K and HDAC inhibitor, CUDC-907, effectively inhibits endometrial cancer growthFrontiers in oncology · 2025Article
- Intestinal NUCB2/nesfatin-1 regulates hepatic glucose production via the MC4R-cAMP-GLP-1 pathway.The EMBO journal · 2025Article
- Analyzing and Validating the Role of Genes Related to Glucagon-like Peptide-1 Signaling in the Prognosis of Pancreatic Cancer.Current medicinal chemistry · 2025Article
- Article
- Aberrant expression of MRAS and HEG1 as the biomarkers for osimertinib resistance in LUAD.Discover oncology · 2024Article
- G9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1.Cell death & disease · 2024Article
- Ononin inhibits triple-negative breast cancer lung metastasis by targeting the EGFR-mediated PI3K/Akt/mTOR pathway.Science China. Life sciences · 2024Article
- Long noncoding RNA and messenger RNA profiling in epicardial adipose tissue of patients with new-onset postoperative atrial fibrillation after coronary artery bypass grafting.European journal of medical research · 2024Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G-protein gamma subunit 2 (GNG2) is involved in several cell signaling pathways, and is essential for cell proliferation and angiogenesis. However, the role of GNG2 in tumorigenesis and development remains unclear. In this study, 1321 differentially expressed genes (DEGs) in breast cancer (BC) tissues were screened using the GEO and TCGA databases. KEGG enrichment analysis showed that most of the enriched genes were part of the PI3K-Akt signaling pathway. We identified GNG2 from the first five DEGs, its expression was markedly reduced in all BC subtype tissues. Cox regression analysis showed that GNG2 was independently associated with overall survival in patients with luminal A and triple-negative breast cancers (TNBC). GNG2 over-expression could significantly block the cell cycle, inhibit proliferation, and promote apoptosis in BC cells in vitro. In animal studies, GNG2 over-expression inhibited the growth of BC cells. Further, we found that GNG2 significantly inhibited the activity of ERK and Akt in an MRAS-dependent manner. Importantly, GNG2 and muscle RAS oncogene homolog (MRAS) were co-localized in the cell membrane, and the fluorescence resonance energy transfer (FRET) experiment revealed that they had direct interaction. In conclusion, the interaction between GNG2 and MRAS likely inhibits Akt and ERK activity, promoting apoptosis and suppressing proliferation in BC cells. Increasing GNG2 expression or disrupting the GNG2-MRAS interaction in vivo could therefore be a potential therapeutic strategy to treat BC.
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