ArticleOncogene2018
microRNA-200a downregulation in human glioma leads to Gαi1 over-expression, Akt activation, and cell proliferation.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 110 citations in OpenAlex.
- Development and validation of a DYX1C1- and GNAI1-based nomogram for predicting relapse in HER2-positive breast cancer treated with trastuzumab.Translational cancer research · 2026Article
- FSTL4 interaction with Gαi proteins activates the Akt-mTOR pathway to drive malignant phenotypes in non-small cell lung cancer.Cell communication and signaling : CCS · 2026Article
- SPOCK1 acts as a negative regulator of ferroptosis in non-small cell lung cancer.NPJ precision oncology · 2026Article
- NLGN3 contributes to angiogenesis in myocardial infarction via activation of the Gαi1/3-Akt pathway.Basic research in cardiology · 2026Article
- Mitochondrial complex I subunit NDUFS4 overexpression drives glioma progression by regulating mitochondrial function and COX5B.NPJ precision oncology · 2026Article
- MicroRNA-based integrated diagnosis and therapy for GBM: current status and advances.Frontiers in immunology · 2026Review
- Endothelial RAB5IF is required for pathological and developmental retinal angiogenesis.Nature communications · 2025Article
- Identification of Gαi1 as a key regulator of tumor progression in nasopharyngeal carcinoma.Discover oncology · 2025Article
- Gap junction protein beta 5 interacts with Gαi3 to promote Akt activation and cervical cancer cell growth.Cell death & disease · 2025Article
- Gαi3: a crucial biomarker and therapeutic target in bladder cancer.NPJ precision oncology · 2025Article
- miR-200 family as new potential prognostic factor of overall survival of patients with WHO G2 and WHO G3 brain gliomas.Scientific reports · 2024Article
- COL8A1 overexpression promotes glioma cell growth by activating focal adhesion kinase signaling cascade.NPJ precision oncology · 2024Article
- The critical role of Gαi3 in oral squamous cell carcinoma cell growth.Cell death discovery · 2024Article
- Identification of Gαi3 as a promising molecular oncotarget of pancreatic cancer.Cell death & disease · 2024Article
- Origin recognition complex 6 overexpression promotes growth of glioma cells.Cell death & disease · 2024Article
- Identification of the central role of RNA polymerase mitochondrial for angiogenesis.Cell communication and signaling : CCS · 2024Article
- Expression and functional implications of YME1L in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Increased expression of REG3A promotes tumorigenic behavior in triple negative breast cancer cells.Breast cancer research : BCR · 2024Article
- Targeting the mitochondrial protein YME1L to inhibit osteosarcoma cell growth in vitro and in vivo.Cell death & disease · 2024Article
- Expression and functional significance of phosphoenolpyruvate carboxykinase 1 in uveal melanoma.Cell death discovery · 2024Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously identified a pivotal role for G protein α inhibitory subunit 1 (Gαi1) in mediating PI3K-Akt signaling by receptor tyrosine kinases (RTKs). Here, we examined the expression and biological function of Gαi1 in human glioma. Gαi1 mRNA and protein expression were significantly upregulated in human glioma tissues, which correlated with downregulation of an anti-Gαi1 miRNA: microRNA-200a ("miR-200a"). Forced-expression of miR-200a in established (A172/U251MG lines) and primary (patient-derived) human glioma cells resulted in Gαi1 downregulation, Akt inactivation and proliferation inhibition. Reduction of Gαi1 expression by shRNA, dominant negative mutant interference, or complete Gαi1 depletion inhibited Akt activation and cell proliferation. Notably, miR-200a was unable to inhibit glioma cell proliferation when Gαi1 was silenced or mutated. Co-immunoprecipitation studies, in human glioma cells and tissues, show that Gαi1 forms a complex with multiple RTKs (EGFR, PDGFRα, and FGFR) and the adapter protein Gab1. In vivo, the growth of subcutaneous and orthotopic glioma xenografts in nude mice was largely inhibited by expression of Gαi1 shRNA or miRNA-200a. Collectively, miR-200a downregulation in human glioma leads to Gαi1 over-expression, Akt activation and glioma cell proliferation.
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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.