The lncRNA LINC00675 regulates cell proliferation, migration, and invasion by affecting Wnt/β-catenin signaling in cervical cancer

Cervical cancer is one of the most common gynecological malignancies worldwide. Recently, the long noncoding RNAs (lncRNAs) have been shown to play essential roles in cervical cancer development and progression. This study investigated the role of lncRNA LINC00675 in cervical cancer and explored the relevant molecular mechanisms. LINC00675 expression was determined by quantitative real-time polymerase chain reaction; cell proliferation, migration and invasion were determined by Cell Counting Kit-8, Transwell migration, and invasion assays, respectively; cell apoptosis was measured by flow cytometry; protein levels were measured by western blot assay. LINC00675 was upregulated in the cervical cancer tissues and cell lines, and upregulation of LINC00675 was positively correlated with advanced clinical stage and poor prognosis in patients with cervical cancer. Overexpression of LINC00675 promoted cervical cancer cell proliferation, invasion, and migration. In addition, overexpression of LINC00675 inhibited cell apoptosis, increased the protein level of Bcl-2, and decreased the protein level of Bax in cervical cancer cells. However, knockdown of LINC00675 played a contrasting role in cervical cancer cells. Overexpression of LINC00675 also increased the activity of Wnt/beta-catenin signaling in cervical cancer cells, whereas knockdown of LINC00675 suppressed the activity of Wnt/beta-catenin signaling. In addition, lithium chloride treatment attenuated the effects of LIC00675 knockdown on CaSki cell proliferation, invasion and migration. In vivo tumor growth study showed that knockdown of LINC00675 suppressed tumor growth, increased the protein levels of Bax and GSK-3 beta, and decreased the protein levels of Bcl-2 and beta-catenin in isolated tumor tissues. In conclusion, our results implied that LINC00675 promoted cancer cell proliferation, migration, and invasion, and inhibit apoptosis likely by modulating the Wnt/beta-catenin pathway.