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Introduction
Non-small cell lung cancer (NSCLC) accounts for approximately 80% of all lung cancers, which are the primary cause of cancer-related deaths worldwide [1]. Despite advances in the early diagnosis and treatment of lung cancer, the prognosis of lung cancer patients remain poor, with the five-year overall survival rates currently at 18% [2]. Hence, an improved and detailed understanding of the molecular mechanisms underlying NSCLC progression is desperately needed. Recently, increasing evidence has shown that long non-coding RNAs (lncRNAs) provide new insights into the treatment of NSCLC pathogenesis.
Protein-coding genes account for only 2% of the human genome, whereas the vast majority of transcripts are non-coding RNAs (ncRNAs), including microRNA (miRNAs) and lncRNAs [3]. A number of microRNAs were found to act as oncogenes or tumor suppressor genes by previous reports [4], whereas the mechanism of action for long ncRNAs (lncRNAs) remains largely unknown. LncRNAs are a class of non-coding RNA greater than 200 nucleotides with no protein-coding potential [5]. LncRNAs play critical roles in numerous biological processes, such as epigenetic regulation, nuclear import, cell cycle control, imprinting, differentiation, alternative splicing, RNA decay and transcription [6, 7]. Recent studies have revealed that the expression of lncRNAs is frequently dysregulated in cancers including NSCLC, and is usually correlated with cancer progression, metastasis and poor prognosis [8, 9]. For example, Wan et al. found that the lncRNA plasmacytoma variant translocation 1 (PVT1) promoted NSCLC proliferation by epigenetically regulating large tumor suppressor kinase 2 (LATS2) expression [10]. LncRNA- urothelial carcinoma-associated 1 (UCA1) exerts oncogenic functions in NSCLC by targeting miR-193a-3p [11]. A complete understanding of the roles of lncRNAs in NSCLC would greatly advance the development of novel therapeutic strategies.
The lncRNA XIST (X-inactive specific transcript), a product of the XIST gene, is the master regulator of X inactivation in mammals, and XIST is exclusively transcribed from the inactive X chromosome [12]. XIST is highly expressed in some carcinomas including breast cancer [13], glioblastoma [14] and ovarian cancer [15], suggesting that XIST may serve as a biomarker for the diagnosis of these cancers. A recent study showed that XIST is upregulated and is essential for the long term survival of NSCLC [16]; however, its molecular role in NSCLC has not been clarified.
In this study, we first...