<p>The LINC01260 Functions as a Tumor Suppressor via the miR-562/CYLD/NF-κB Pathway in Non-Small Cell Lung Cancer</p>
Authors: Shihui Sun
Xing Lin
Yujie Lei
Kai Chen
Yunchao Huang
Yangming Chen
Jiguang Zhang
Jianbin Lin
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: CYLD; long noncoding RNA; miR-562; non-small cell lung cancer.
Affiliations: Department of Thoracic Surgery, Shengli Clinical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou, Fujian 350001, People's Republic of China., Department of Thoracic Surgery I, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Yunnan Cancer Center, The International Cooperation Key Laboratory of Regional Tumor in High Altitude Area, Kunming, Yunnan 650106, People's Republic of China.

Abstract:  Purpose: Recently, long noncoding RNAs (lncRNAs) have been identified as novel and potential therapeutic targets in various cancer types. Nonetheless, the levels and biological effects of lncRNAs in non-small cell lung cancer (NSCLC) remain largely unknown. In this study, we aimed to identify the effects of lncRNA-LINC01260 throughout the progression of NSCLC and explore the underlying mechanism. Methods: Quantitative real-time PCR (qRT-PCR) and Western blot were performed to measure LINC01260, miR-562, and CYLD expression and protein levels. Luciferase reporter assay was employed to investigate the relationship between LINC01260 and miR-562, and miR-562 and CYLD, respectively. The viability and migration of cells were evaluated using CCK-8, colony formation, and transwell assays. The effects of LINC01260 were identified through tumorigenesis in vivo. ELISA was performed to detect the activity of NF-κB and p65 expression. Results: In NSCLC tissues and cell lines, LINC01260 expression was downregulated, which corresponded to a lower survival rate of patients with NSCLC. Knockdown of LINC01260 accelerated the proliferation, colony formation, and migration of NSCLC cells. Moreover, downregulation of LINC01260 inhibited apoptosis of NSCLC cells by regulating the expression of Bcl-2 and Bax proteins in vitro. In vivo, the downregulation of LINC01260 promoted tumor growth. miR-562 was identified as the target gene of LINC01260, which was upregulated in NSCLC tumors. Furthermore, CYLD was identified as the target gene of miR-562. The effects of LINC01260 were exerted by regulating CYLD via sponging miR-562. ELISA confirmed that the upregulation of CYLD inhibited NF-κB activity; however, the co-transfection of sh-LINC01260 partly reversed the inhibition. Additionally, CYLD reduced p65 expression; however, downregulation of LINC01260 slightly increased the expression level. Conclusion: This study revealed a novel LINC01260/miR-562/CYLD/NF-κB pathway in the pathogenesis of NSCLC and suggested a potential therapeutic target for NSCLC. 

Retracted: No

PubPeer comments:
  We obtained NSCLC and NSCLC-adjacent tissue (u22643 cm) samples from 32 patients with NSCLC who had undergone surgery at Shengli Clinical College of Fujian Medical University, Fujian Provincial Hospital from **January 2016 to June 2018**. Fig 1F.  Survival analysis showed that a low expression of LINC01260 was a predictor of a worse prognosis, R2 =0.4097, P=0.0085 . ![file] The authors evidently followed the survival of their patients for 12 or 13 years after surgery, i.e. up to a date range of **2028 to 2030**. How does that work? ,