Abstract

Introduction: LINK-A lncRNA is a well-characterized oncogenic lncRNA only in triple negative breast cancer. Our study was carried out to investigate the possible involvement of LINK-A lncRNA in ovarian carcinoma. Methods: Expression of LINK-A in ovarian biopsies and plasma of both ovarian carcinoma patients and healthy females was detected by qRT-PCR. Plasma TGF-β1 was detected by ELISA. Correlation between plasma LINK-A and TGF-β1 was analyzed by Pearson correlation analysis. Correlation between plasma LINK-A and patients’ clinicopathological data was analyzed by Chi-square test. LINK-A overexpression vector was transfected into cells of human ovarian carcinoma cell lines. Cell migration and invasion were detected by Transwell migration and invasion assay. TGF-β1 expression was detected by Western blot. Results: We found that LINK-A and TGF-β1 were up-regulated in ovarian carcinoma patients than in healthy controls. Plasma levels of LINK-A were positively correlated with plasma TGF-β1 in ovarian carcinoma patients but not in healthy controls. Plasma levels of LINK-A were correlated with distant tumor metastasis but not tumor size. LINK-A overexpression led to up-regulated TGF-β1 in ovarian carcinoma cells and promoted cell migration and invasion. In contrast, TGF-β1 treatment showed no effects on LINK-A expression but attenuated the effects of LINK-A overexpression on cell migration and invasion. Conclusions: We conclude that LINK-A lncRNA may promote migration and invasion of ovarian carcinoma cells by activating TGF-β pathway.

Highlights

  • LINK-A lncRNA is a well-characterized oncogenic lncRNA only in triple negative breast cancer

  • Plasma levels of TGF-β1 were higher in patients with ovarian carcinoma than in healthy females

  • Plasma levels of LINK-A are positively correlated with plasma levels of TGF-β1 in ovarian carcinoma patients but not in healthy females

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Summary

Introduction

LINK-A lncRNA is a well-characterized oncogenic lncRNA only in triple negative breast cancer. Methods: Expression of LINK-A in ovarian biopsies and plasma of both ovarian carcinoma patients and healthy females was detected by qRT-PCR. Results: We found that LINK-A and TGF-β1 were up-regulated in ovarian carcinoma patients than in healthy controls. Plasma levels of LINK-A were positively correlated with plasma TGF-β1 in ovarian carcinoma patients but not in healthy controls. Plasma levels of LINK-A were correlated with distant tumor metastasis but not tumor size. LINK-A overexpression led to up-regulated TGF-β1 in ovarian carcinoma cells and promoted cell migration and invasion. TGF-β1 treatment showed no effects on LINK-A expression but attenuated the effects of LINK-A overexpression on cell migration and invasion. Conclusions: We conclude that LINK-A lncRNA may promote migration and invasion of ovarian carcinoma cells by activating TGF-β pathway.

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