miR-145 regulates proliferation and chemotherapy sensitivity of ovarian carcinoma

Previous work showed that miR-145 is downregulated in human serous epithelia ovarian carcinoma (SEOC) tissue and SKOV3 cells. However, the molecular mechanisms of miR-145 used to regulate ovarian proliferation and chemotherapy sensitivity remain to be determined. The present research demonstrate that miR-145 inhibit SKOV3 cells proliferation and promote chemotherapy sensitivity to paclitaxel according to MTT assay. MiR-145 inhibits Mucin1 (MUC1) post-transcriptional expression by binding to its 3'-untranslated region (UTR). The epithelial mesenchymal transition (EMT) marker E-cadherin (E-cad), which is downstream molecule of MUC1, is promoted by miR-145 overexpression. Furthermore, the E-cad protein level is inversely correlated with the expression of MUC1 in SKOV3 cells. It showed that promotion of E-cad signaling induced by miR-145 was released by MUC1 inhibition. Taken together, miR-145 serves as a tumor suppressor which can upregulate E-cad expression by targeting MUC1, leading to the inhibition of tumor proliferation and chemotherapy sensitivity. The miR-145 could be a rationale for therapeutic applications in ovarian carcinoma in the future.

Ovarian carcinoma; miR-145; MUC1; Proliferation; Chemotherapy sensitivity.

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