Long non‑coding RNA SNHG20 promotes ovarian cancer development by targeting microRNA‑338‑3p to regulate MCL1 expression
- Ding Wang
- Zhiying Li
- Hui Li
- Jiao Lu
- Qi Qin
Affiliations: Department of Gynecology, The Affiliated Renhe Hospital of China Three Gorges University, Yichang, Hubei 443001, P.R. China
- Published online on: December 18, 2020 https://doi.org/10.3892/ol.2020.12391
Copyright: © Wang
et al. This is an open access article distributed under the
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Long non‑coding RNAs (lncRNAs) and microRNAs (miRNAs/miRs) were reported to be associated with the development of ovarian cancer (OC). Increasing evidence demonstrated that lncRNA SNHG20 and miR‑338‑3p were involved in OC. However, the functional mechanism of lncRNA SNHG20 and miR‑338‑3p in OC development remains unknown. The expression of SNHG20, miR‑338‑3p and myeloid cell leukemia 1 (MCL1) was detected by reverse transcription‑quantitative PCR. MTT assay, flow cytometry and transwell migration and invasion assays were used to assess cell proliferation, apoptosis, migration and invasion, respectively. The relative protein expression was detected by western blot analysis. The interaction between miR‑338‑3p and SNHG20 or MCL1 was predicted by starBase v3.0, and subsequently confirmed by dual‑luciferase reporter assay. Besides, mouse xenograft assay was carried out to explore the effect of SNHG20 on tumor growth in vivo. The levels of SNHG20 and MCL1 were upregulated, while miR‑338‑3p level was downregulated in OC tissues and cells. SNHG20 knockdown repressed OC cell proliferation, migration, invasion and epithelial‑mesenchymal transition, and induced apoptosis. Interestingly, SNHG20 targeted miR‑338‑3p to regulate MCL1 expression. miR‑338‑3p depletion or MCL1 overexpression could reverse the effects of SNHG20 knockdown on OC cells. Besides, SNHG20 knockdown impeded tumor growth in vivo. In conclusion, the present study demonstrated that SNHG20 regulates OC development via modulation of the miR‑338‑3p/MCL1 axis, providing the theoretical basis for the treatment of OC.