ArticleTranslational cancer research2021
MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway.
Article in Translational cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Dual Inhibition of PI3K-AKT Signaling Pathway by miR-542 Overexpression in Cervical Cancer.Biochemical genetics · 2026Article
- Review
- Effects of Notch signaling on proliferation, angiogenesis, and adipogenesis of hemangioma-derived stem cells.European journal of histochemistry : EJH · 2025Article
- Human papillomavirus-mediated cervical cancer: epigenetic interplay and clinical implications.Frontiers in microbiology · 2025Review
- [Notch1/Akt/Foxo1 Pathway Regulated by Kisspeptin Is Involved in Endometrial Decidualization in Patients With Recurrent Spontaneous Abortion].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Article
- Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCervical cancer (CC) is frequently diagnosed, and accounts for a large proportion of cancer-related mortality worldwide. Therefore, it is an urgent need to explore the mechanisms of CC progression and seek new therapeutic targets. We know that microRNA-137 (miR-137) is involved in CC progression; however, it's mechanism in CC has not yet been clarified.
methodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expressions of miR-137 and Notch homolog 1 messenger RNA (Notch1 mRNA) in CC cells. Cell Counting Kit-8 (CCK-8) and Transwell assay were utilized to monitor the proliferation, invasion, and migration of CC cells. The binding relationship of miR-137 with Notch1 was detected by dual luciferase reporter gene assay. Western blot was used to determine the expressions of Notch1, p-AKT/AKT, and p-mTOR/mTOR signaling pathways.
resultsThe results showed that miR-137 was down-regulated and Notch1 was up-regulated in CC cells. MiR-137 was reversely correlated with Notch1, and Notch1 partially reversed the promotion of miR-137 silencing on malignant phenotype of CC cells. Furthermore, in vitro experiments confirmed that miR-137 partially impeded CC progression via regulation of the Notch1 and PI3K/AKT/mTOR axis.
conclusionsMiR-137 targets Notch1 and regulates CC through the PI3K/Akt/mTOR pathway. The miR-137/Notch1 axis may be a promising target for CC patients, and these findings can provide a reference for the clinical treatment of CC.
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