Abstract
The initiation and development of several types of cancer have been linked to long non‑coding RNA (lncRNA) X inactive‑specific transcript (XIST). Yet, the pattern of expression, function, as well as the molecular mechanism underlying XIST in laryngeal squamous cell carcinoma (LSCC) lack characterization. Therefore, the present study aimed to determine the function and putative mechanism of XIST in the development of LSCC. It was revealed that the level of XIST was significantly higher in LSCC tissues that were associated with advanced Tumor‑Node‑Metastasis (TNM) stage and the presence of lymph node metastasis. Furthermore, the ability of human LSCC TU212 cells to proliferate, form colonies, migrate and invade was significantly suppressed, while cell apoptosis was significantly increased following knockdown of XIST. Further investigation revealed that XIST knockdown increased the expression of microRNA‑144 (miR‑144) by acting as an endogenous sponge of miR‑144. Inhibition of miR‑144 caused a partial reversal of the inhibitory effects mediated following depletion of XIST in LSCC cells. Moreover, an miR‑144 target called insulin receptor substrate 1 (IRS1) was significantly decreased by XIST depletion in LSCC cells. IRS1 expression was positively correlated with XIST expression in LSCC tissues. In addition, knockdown of XIST impaired tumor growth in vivo by regulating the miR‑144/IRS1 axis. The present study demonstrated that the progression of LSCC is promoted by XIST sponging miR‑144 to regulate IRS1 expression, suggesting that XIST can serve as a putative target in the therapy of LSCC.