Abstract

The long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) acts as an oncogene in several cancers, and is highly expressed in ovarian cancer. MiR-543, a tumor suppressor, was expressed lowly in ovarian cancer. However, whether SNHG6 performed its oncogenic role via miR-543 in ovarian cancer, as well as the underlying mechanism is still not clear. In this study, we showed that the levels of SNHG6 and Yes-associated protein 1 (YAP1) were significantly elevated, while the level of miR-543 was significantly decreased, in ovarian cancer tissues compared with adjacent normal samples. We demonstrated that overexpression of SNHG6 significantly promoted the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of ovarian cancer cells SKOV3 and A2780. Knockdown of SNHG6 showed the opposite effects. MiR-543 level was negatively correlated with the SNHG6 level in ovarian cancer tissues. SHNG6 overexpression significantly inhibited the expression of miR-543, and SHNG6 knockdown significantly elevated the expression of miR-543 in ovarian cancer cells. The effects of SNHG6 on ovarian cancer cells were abrogated by miR-543 mimic, and strengthened by anti-miR-543. YAP1 was identified as a target of miR-543. Forced expression of miR-543 significantly inhibited the expression of YAP1. Moreover, YAP1 overexpression could reverse the effects of SNHG6 downregulation on the malignant phenotypes of ovarian cancer cells. In summary, our study showed that SNHG6 promoted the malignant phenotypes of ovarian cancer cells via miR-543/YAP1 pathway.

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