ArticleCancer biomarkers : section A of Disease markers2017
MicroRNA-937 inhibits cell proliferation and metastasis in gastric cancer cells by downregulating FOXL2.
Article in Cancer biomarkers : section A of Disease markers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Cepharanthine inhibits the proliferation and epithelial-mesenchymal transition of oral squamous cell carcinoma via HMGA2/FOXL2 axis.BMC pharmacology & toxicology · 2025Article
- Role of Fork-Head Box Genes in Breast Cancer: From Drug Resistance to Therapeutic Targets.Biomedicines · 2023Review
- Forkhead box L2 is a target of miR-133b and plays an important role in the pathogenesis of non-small cell lung cancer.Cancer medicine · 2023Article
- Circular RNA expression profiles and CircSnd1-miR-135b/c-foxl2 axis analysis in gonadal differentiation of protogynous hermaphroditic ricefield eel Monopterus albus.BMC genomics · 2022Article
- Identification and Characterization of MicroRNAs Involving in Initial Sex Differentiation ofBiology · 2022Article
- Identification of miRNA signature for predicting the prognostic biomarker of squamous cell lung carcinoma.PloS one · 2022Article
- MiR-139-5p Inhibits the Development of Gastric Cancer through Targeting TPD52.Journal of healthcare engineering · 2022Article
- MicroRNA-937 is overexpressed and predicts poor prognosis in patients with colon cancer.Diagnostic pathology · 2019Article
- New STAT3-FOXL2 pathway and its function in cancer cells.BMC molecular and cell biology · 2019Article
- Oncogenic Role and Prognostic Value of MicroRNA-937-3p in Patients with Breast Cancer.OncoTargets and therapy · 2019Article
- MicroRNA-937 inhibits the malignant phenotypes of breast cancer by directly targeting and downregulating forkhead box Q1.OncoTargets and therapy · 2019Article
- miR-937 regulates the proliferation and apoptosis via targeting APAF1 in breast cancer.OncoTargets and therapy · 2019Article
Corrections and comments
- Retraction · 2020-09-25Investigation by Third Party · Notice - Limited or No Information · Paper Mill · Removed · · see also: https://scienceintegritydigest.com/2020/02/21/the-tadpole-paper-mill/
- Retracted
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite advancement in the treatment, the mortality of gastric cancer remains high. MicroRNAs (miRNAs) are involved in tumor development and progression by regulating signaling pathways. In this study, we investigated the role of miR-937 in gastric cancer cells.
methodsMiR-937 expression was determined in gastric cancer and matched normal tissues, and human gastric cancer cell lines by quantitative real-time PCR (qRT-PCR). Effects of miR-937 on cell proliferation, migration and invasion were analyzed by MTT and Transwell assays, respectively. In addition, the regulation of FOXL2 by miR-937 was evaluated by western blotting and luciferase reporter assays. Effects of FOXL2 on cell proliferation, migration and invasion were detected again.
resultsMiR-937 level was low expressed in gastric cancer tissues and cell lines. Overexpression of miR-937 inhibited cell viability, colony formation and promoted apoptosis in gastric cancer cells. MiR-937 overexpression also inhibited cell migration and invasion by inhibiting the EMT process. Furthermore, we found that FOXL2 was a direct target of miR-937 and negatively regulated by miR-937. Moreover, miR-937 overexpression inhibited the activation of the PI3K/AKT pathway. Furthermore, we found that overexpression of FOXL2 promoted cell viability, colony formation, migration, invasion, and inhibited apoptosis in gastric cancer cells.
conclusionsMiR-937 inhibits the proliferation and metastasis of gastric cancer cells by targeting FOXL2 via inactivation of PI3K/AKT signaling pathway. These results suggest that miR-937 may be a potential target for the treatment of gastric cancer.
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