X-inactive specific transcript (XIST), one of the first found
cancer-associated long non-coding RNAs (lncRNAs), is involved in the development and progression of many types of
tumors. Aberrant expression of XIST has been observed in
hepatocellular carcinoma, cervical, breast, ovarian and
colorectal cancer. However, the exact effects and molecular mechanisms of XIST in
lung cancer progression are still unknown to date. In the present study, we investigated the role of XIST in human
lung cancer cell lines and clinical
tumor samples in order to determine the function of this molecule. In our research,
lncRNA-XIST was specifically upregulated in
lung cancer cell lines and promoted
lung cancer cell growth through targeting miR-140. Knockdown of XIST inhibited the proliferation and promoted cell apoptosis of human
lung cancer cells and suppressed
metastasis in vitro and in vivo. In addition, miR-140-dependent inhibitor of apoptosis-stimulating
protein of p53 (iASPP) regulation was required in XIST-induced
lung cancer cell growth. These findings indicated that XIST may regulate the
tumor growth and
metastasis via miR-140-dependent iASPP regulation. Taken together, our data indicated that XIST may be an oncogenic
lncRNA that promotes the proliferation and
metastasis of
lung cancer through the regulation of miR-140 and could be regarded as a therapeutic target in human
lung cancer.