ArticleMolecular and cellular biochemistry2018
ARHGEF39 promotes gastric cancer cell proliferation and migration via Akt signaling pathway.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Multiomics profiling of zebrafish embryonic cell line PAC2 across growth phases to assess its relevance for toxicological studies.PloS one · 2026Article
- DeepCBS: shedding light on the impact of mutations occurring at CTCF binding sites.Frontiers in genetics · 2024Article
- ARHGEF3 regulates the stability of ACLY to promote the proliferation of lung cancer.Cell death & disease · 2022Article
- Article
- Identification of cuproptosis-related gene signature to predict prognosis in lung adenocarcinoma.Frontiers in genetics · 2022Article
- Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway.Genetics and molecular biology · 2020Article
- Expression of Rho Guanine Nucleotide Exchange Factor 39 (ARHGEF39) and Its Prognostic Significance in Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Comprehensive investigation of alternative splicing and development of a prognostic risk score for prostate cancer based on six-gene signatures.Journal of Cancer · 2019Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Dbl-family guanine nucleotide exchange factors (GEFs) can activate RhoGTPases by facilitating the exchange of GDP for GTP, the aberrant expression of which has been implicated in tumorigenicity and metastasis of human cancers. ARHGEF39, as a member of Dbl-family GEFs, was reported to be a potential oncogene in human hepatocellular carcinoma previously. However, the role of ARHGEF39 in gastric cancer (GC) remains unclear so far. In the current study, we demonstrated that ARHGEF39 expression was significantly upregulated in GC tissues compared with paired adjacent normal tissues by quantitative real-time PCR analysis. Functional analyses revealed that ARHGEF39 overexpression could promote proliferation, colony formation, and migration of GC cells in vitro, whereas ARHGEF39 knockdown markedly suppressed these phenotypes. Moreover, ARHGEF39 enhanced tumorigenicity and lung metastasis potential of GC cells in nude mice model. Mechanistically, we found that overexpressed ARHGEF39 significantly increased the phosphorylation level of Akt (p-Akt), and its effect on cell proliferation was attenuated by PI3K inhibitor LY294002. Thus, our findings suggest that ARHGEF39 may contribute to cell proliferation and migration in GC via a possible mechanism involving Akt signaling.
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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 Socratic graph.