miR‑638 suppresses proliferation by negatively regulating high mobility group A1 in ovarian cancer cells
- Li Ma
- Wei Zhang
- Yaofeng Jin
- Xiaomei Bai
- Qiaoling Yu
Affiliations: Department of Pathology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China, Department of Scientific Research, The First Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi 710077, P.R. China
- Published online on: September 20, 2021 https://doi.org/10.3892/etm.2021.10754
Copyright: © Ma
et al. This is an open access article distributed under the
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Ovarian cancer is one of the most common gynecological diseases with high mortality rates. Previous studies have shown that microRNA (miR)‑638 is associated with tumorigenesis. The present study aimed to assess the role and underlying mechanisms of miR‑638 in ovarian cancer. miR‑638 expression was detected in ovarian cancer tissues and miR‑638 was overexpressed or knocked down in ovarian cancer OVCAR‑3 and Caov‑3 cells. The clinical results revealed that miR‑638 expression was downregulated in ovarian cancer tissues compared with in adjacent normal tissues. miR‑638 expression was also found to be relatively low in OVCAR‑3 cells whilst being relatively high in Caov‑3 cells among the five ovarian cancer cell lines tested. miR‑638 overexpression inhibited cell viability, arrested the cell cycle at the G1 phase and promoted apoptosis in OVCAR‑3 cells. By contrast, miR‑638 knockdown increased Caov‑3 cell viability, facilitated cell cycle progression and inhibited apoptosis. miR‑638 reduced the expression of high mobility group A1 (HMGA1) by directly targeting its 3' untranslated region. HMGA1 overexpression reversed the inhibition of proliferation induced by miR‑638 overexpression in OVCAR‑3 cells. These results suggest that miR‑638 may serve to be a suppressor of ovarian cancer by regulating HMGA1, which may provide a potential therapeutic target for ovarian cancer.