Abstract
ObjectiveHigh-grade serous ovarian cancer (HGSOC) is an aggressive gynaecological malignancy and associated with poor prognosis. Here we examined the effects of miR-625-3p on proliferation, treatment, migration and invasion in HGSOC.MethodsThe proliferation of HGSOC cells was evaluated by MTT assay. Transwell assay was performed to examine migration and matrigel assay were used to assess invasion. The effect of miR-625-3p on cisplatin-induced apoptosis was investigated by Caspase-Glo3/7 assay. The dual-luciferase reporter assay was carried out to confirm the potential binding site.ResultsOverexpression of miR-625-3p promoted proliferation, and increased migration and invasion in HGSOC cells. MiR-625-3p significantly inhibited cisplatin sensitivity in HGSOC cells. Meanwhile, miR-625-3p decreased cisplatin-induced apoptosis by regulation of BAX and Bcl-2 expression. Furthermore, aberrant expression of miR-625-3p changed PTEN expression by directly binding to 3’UTR of PTEN. Further study showed miR-625-3p expression was higher in human HGSOC tissue than normal ovarian tissues and associated with higher clinical stage.ConclusionsmiR-625-3p promotes HGSOC growth, involves chemotherapy resistance and might serve as a potential biomarker to predict chemotherapy response and prognosis in HGSOC.
Highlights
High-grade serous ovarian cancer (HGSOC) is consisted of 60-80% of ovarian epithelial carcinoma, and patients with HGSOC most often present at advanced clinical stage and have poor outcome [1]
We evaluated the effects of miR-625-3p in growth, cisplatin sensitivity, migration and invasion using HGSOC cells and tissue
MiR‐625‐3p increased growth of OVCAR3 and OVCAR4 and inhibited cisplatin sensitivity miR-625-3p expression was dramatically increased in OVCAR3 (Fig. 1A) and OVCAR4 (Fig. 1C) cells after transfection of miR-625-3p mimic
Summary
HGSOC is consisted of 60-80% of ovarian epithelial carcinoma, and patients with HGSOC most often present at advanced clinical stage and have poor outcome [1]. The first-line treatment of HGSOC is debulking surgery followed by chemotherapy [2]. Cisplatin interferes cell division and inhibits cancer cell proliferation, and has been used as a chemotherapy reagent for a variety of cancers including HGSOC [3]. Studies have shown that cancer cells develop cisplatin resistance by reducing accumulation [4, 5]. Patients who develop cisplatin resistance often have shorter survival time.
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