MicroRNAs (miRNAs) are a group of small non-coding RNAs that modulate post-transcriptional gene expression. It has been demonstrated that various miRNAs may be expressed at different levels in different types of tumors. The present study assessed the role of microRNA-148a-3p (miR-148a-3p) in epithelial ovarian cancer (EOC). The results demonstrated that miR-148a-3p was decreased in EOC tissues and that a lower miRa-148-3p concentration was associated with a higher overall survival rate. Transfection of miR-148a-3p suppressed the invasive and proliferative capacity of SKOV3 cells. The induced overexpression of miR-148a-3p significantly inhibited the relative luciferase activity of the pmirGLO-c-Met-3′untranslated region compared with an empty vector. In addition, c-Met silencing led to a decrease in the invasive and proliferative capacity of EOC cells. The inhibition of miR-148a-3p did not increase the invasiveness of SKOV3 cells, even when c-Met was silenced. To the best of our knowledge, the present study is the first to demonstrate that miR-148a-3p expression is decreased in EOC cancer tissues and cell lines. The present study therefore demonstrated that miR-148a-3p may serve as a tumor suppressor in EOC by targeting c-Met.

Objective: To describe the clinical and pathological features of endometrial carcinoma with extraperitoneal metastasis and examine whether surgery could improve the prognosis. Methods: The Surveillance, Epidemiology, and End Results database was used to analyze 730 patients who were diagnosed with extraperitoneal metastasis of endometrial cancer from 2010 to 2015, including metastasis to the lung, bone, or brain. Results: Of the 730 patients, 372 (50.96%) patients had single lung metastases, and 196(26.85%) patients had multiple organ metastases that included pulmonary invasion. Therefore, the lung was the most common target organ for extraperitoneal metastasis of endometrial cancer. In multivariate risk factor analysis, grade 3 tumor (odds ratio = 3.39, P < .001), positive peritoneal cytology (odds ratio = 2.02, P < .001), and cervical stromal invasion (odds ratio = 1.42, P = .030) were independent risk factors for extraperitoneal metastasis. Once metastasis occurred in the brain or multiple organs, the prognosis was often poor. Of the patients, 362 underwent surgery, and surgery was performed only for primary tumors of the reproductive organs in almost all patients (97.23%) with extraperitoneal metastasis. The median cancer-specific survival periods of patients with solitary pulmonary metastasis undergoing surgery and those without surgery were 23 (16.43-29.57) months and 9 (6.21-11.79) months, respectively ( P < .001), and survival superiority also existed in patients with bone metastasis (19 vs 8 months, P = .015) and multiple organs metastases (15 vs 4 months, P < .001). However, patients with brain metastasis had the same median survival period in the 2 groups (6 months, P = .146). Conclusions: The lung was the most common target organ for extraperitoneal metastasis in patients with endometrial cancer. Surgery was associated with improved survival in women with extraperitoneal metastasis, except for patients with brain metastasis.

The abnormal expression of microRNAs (miRNAs/miRs) has been widely reported in various tumor types. miR-217 was demonstrated to be aberrantly expressed in a number of tumors, including pancreatic adenocarcinoma and osteosarcoma; however, its specific expression pattern has never been investigated in cervical cancer cells. Compared with normal control, the level of Rho-associated protein kinase 1 (ROCK1) expression was markedly increased in cervical cancer tissues and cells compared with that in non-cancerous tissues and cells. The expression of miR-217 was significantly reduced in cervical cancer tissues and cell lines. Overexpression of miR-217 could suppress colony formation and the cell invasion capacity of SiHa and HeLa cells. Flow cytometry indicated that miR-217 significantly increased cell apoptosis in SiHa and HeLa cells. Dual-luciferase reporter assays demonstrated that ROCK1 was a target gene of miR-217. In addition, overexpression of ROCK1 also led to an increased invasion capacity in SiHa cells, even when miR-217 was inhibited, indicating that the anti-invasive effects of miR-217 were mediated through ROCK1. In summary, the results of the present study indicated that miR-217 functions as a tumor suppressor in cervical cancer cells, primarily by targeting ROCK1.