Long non-coding RNA MALAT1 promotes cholangiocarcinoma cell proliferation and invasion by activating PI3K/Akt pathway.

Abstract

Increasing evidence indicated that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) acted as a key regulator in the proliferation and invasion of several cancers. However, the function of MALAT1 in the development of cholangiocarcinoma has not been experimentally established. In the present study, the expression levels of MALAT1 in cholangiocarcinoma cell lines were detected by quantitative real-time PCR. The effects of MALAT1 knockdown on the cell proliferation and invasion of cholangiocarcinoma cells were detected with Cell Counting Kit-8 (CCK-8), colony formation assay and Trans-well assay, respectively. The expressions of epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin, Vimentin) were evaluated to discover whether the process of EMT was involved. We also evaluated the expression of phos-phatidylinositol-3-kinase/serine/threonine kinase (PI3K/Akt) signaling pathway proteins (PI3K, p-PI3K, Akt, p-Akt) to determine the associated molecular mechanism. And we discovered that MALAT1 was up-regulated in cholangiocarcinoma cancer cells. CCK-8, colony formation and trans-well assay showed that the proliferation and invasion of QBC-939 and RBE with MALAT1 knockdown were inhibited. Moreover, MALAT1 could promote EMT in cholangiocarcinoma cells. In addition, MALAT1 may activate PI3K/Akt pathway. These results indicated that MALAT1 promoted cholangiocarcinoma cell proliferation and invasion. The effects of MALAT1 on cholangiocarcinoma cells might be through activating the PI3K/Akt signaling pathway. These investigations may facilitate a better understanding of MALAT1 and it might be a potential therapeutic target for the treatment of cholangiocarcinoma.