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Background: Discussions regarding the correlations between long non-coding RNAs (lncRNAs) and cancers have dominated research in recent years. SIK1-LNC, a type of lncRNA and adjacent to salt-inducible kinases 1 (SIK1), has been found aberrantly expressed in lung cancer. However, its functional role in lung cancer remains largely unknown., Purpose: In this study, we aimed to explore the association between SIK1-LNC expression and SIK1 in lung cancer cells and further identify the impact of SIK1-LNC on the proliferation, migration invasion of lung cancer cells., Patients and Methods: Of the 30 patients with non-small-cell lung carcinoma from Zhongnan Hospital of Wuhan University, RT-qPCR was performed to detect SIK1 and SIK1-LNC expressions in patients' samples. Overexpression and knockdown experiments were conducted to analyze the SIK1 and SIK1-LNC expressions in lung cancer cell lines. CCK-8, Brdu, scratch wound-healing, and Transwell assays were respectively employed to evaluate the proliferative, migrative, and invasive abilities of lung cancer cells., Results: Both SIK1-LNC and SIK1 expression levels were evidently downregulated in 30 lung cancer tissues. SIK1-LNC expression was bound up with clinicopathologic features, including lymph node metastasis and distant metastasis. SIK1 expression showed a positive tendency with SIK1-LNC expression in lung cancer cells. SIK1-LNC exerted a significant repression on cell proliferatiive, miogrative and invasive abilities of lung cancer cells., Conclusion: Our findings suggested that SIK1-LNC may act as a novel biomarker and therapeutic target for lung cancer., Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Introduction: Echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase ( EML4-ALK ) is identified as an important pathogenic factor in patients with non-small-cell lung cancer (NSCLC) and could induce a stem-like phenotype in NSCLC cells. Crizotinib is commonly used for EML4-ALK + NSCLC treatment, but its acquired resistance results in tumor recurrence. Long intergenic noncoding RNA, regulator of reprogramming (lincROR) is related to the acquisition and maintenance of self-renewal and stemness features of cancer stem cells. It has been documented that lincROR is implicated in chemoresistance. However, the correlations of lincROR and EML4-ALK in stem cell-like properties and of lincROR and crizotinib resistance in NSCLC cells are yet to be elucidated., Patients and Methods: In the present study, we investigated the expression profile of lincROR in EML-ALK NSCLC tissues, and the potential role of lincROR in prognosis was then analyzed. Subsequently, its association with stem cell-like properties of EML-ALK + NSCLC cells was determined. Furthermore, the correlation of lincROR with crizotinib and the effects of lincROR and crizotinib on cell viability of EML4-ALK + NSCLC cells were all explored., Results: The results showed that lincROR expression was upregulated in EML4-ALK + NSCLC tissues relative to EML4-ALK - NSCLC tissues. Low-expressed lincROR was related to a favorable prognosis of patients with EML-ALK NSCLC. lincROR overexpression could enhance the stemness features of EML-ALK + NSCLC cells which were repressed by ALK knockdown., Conclusion: We found that lincROR expression was significantly inhibited because of the increased concentration of crizotinib in EML4-ALK + NSCLC cells. Furthermore, lincROR overexpression increased cell viability of EML4-ALK + NSCLC cells, which was impaired by crizotinib. Conjointly, these results suggested the important role of lincROR in EML-ALK + NSCLC. lincROR may serve as a potential therapeutic target to overcome chemotherapy resistance in EML-ALK + NSCLC., Competing Interests: Disclosure The authors report no conflicts of interest in this work.