ArticleOncology letters2016
Upregulation of PREX2 promotes the proliferation and migration of hepatocellular carcinoma cells via PTEN-AKT signaling.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- AHCYL1 mediates the tumor-promoting effect of PREX2 in non-small cell lung carcinoma.Theranostics · 2025Article
- Whole-Exome Sequencing Reveals Novel Candidate Driver Mutations and Potential Druggable Mutations in Patients with High-Risk Neuroblastoma.Journal of personalized medicine · 2024Article
- Integration of Tumor Heterogeneity for Recurrence Prediction in Patients with Esophageal Squamous Cell Cancer.Cancers · 2021Article
- Phosphatidylinositol 3,4,5-Trisphosphate-Dependent Rac Exchanger 2 Protein Facilitates Glioma Progression via Akt and Stat3 Signaling.Journal of molecular neuroscience : MN · 2021Article
- Integrative analysis of highly mutated genes in hepatitis B virus-related hepatic carcinoma.Cancer medicine · 2020Article
- Identification of P-Rex1 in the Regulation of Liver Cancer Cell Proliferation and Migration via HGF/c-Met/Akt Pathway.OncoTargets and therapy · 2020Article
- Somatic mutations of PREX2 gene in patients with hepatocellular carcinoma.Scientific reports · 2019Article
- Benzo(a)pyrene promotes Hep-G2 cell migration and invasion by upregulating phosphorylated extracellular signal-regulated kinase expression.Oncology letters · 2018Article
- The role of autophagy in hepatocellular carcinoma: friend or foe.Oncotarget · 2017Review
- Identification of DEP domain-containing proteins by a machine learning method and experimental analysis of their expression in human HCC tissues.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphatidylinositol-3,4,5-trisphosphate Rac exchanger 2 (PREX2), a regulator of the small guanosine triphosphatase Rac, demonstrates an inhibitory effect on the activity of phosphatase and tensin homolog (PTEN). Previously, PREX2 was implicated in the regulation of cell invasion in hepatocellular carcinoma (HCC). However, the exact role of PREX2 in the regulation of HCC cell proliferation and migration, as well as the underlying mechanisms, remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction revealed that PREX2 was upregulated in HCC tissue compared with matched adjacent non-tumorous tissue. In addition, the present study demonstrated that the messenger RNA and protein levels of PREX2 increased in human HCC HepG2, LH86, LMH and PLHC-1 cell lines compared with normal human liver THLE-3 cells. Overexpression of PREX2 significantly enhanced the proliferation and migration of HCC cells, and knockdown of PREX2 expression significantly suppressed the proliferation and migration of HCC cells. Additional investigation revealed that overexpression of PREX2 suppressed the activity of PTEN, leading to an enhancement in the activity of protein kinase B (AKT). By contrast, knockdown of PREX2 expression upregulated the activity of PTEN and suppressed the activity of AKT. Overall, the present study suggests that PREX2 promotes the proliferation and migration of HCC cells by inhibiting PTEN-AKT signaling.
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