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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.

Tracheobronchial mucormycosis is a rare but severe disease with high mortality because of its nonspecific clinical presentations and variable predisposing factors.

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