<p>Long Noncoding RNA LINC00460 Facilitates Colorectal Cancer Progression by Negatively Regulating miR-613</p>
Authors: Xinxin Chen
Jian Suo
Xuan Sun
Lei Wang
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: SphK1; colorectal cancer; long noncoding RNA 00460; miR‐613.
Affiliations: Department of Gastrointestinal Surgery, Jilin University First Hospital, Changchun, Jilin 130021, People's Republic of China., Department of Burn Surgery, Jilin University First Hospital, Changchun, Jilin 130021, People's Republic of China.

Abstract:  Background: Long-noncoding RNAs (lncRNAs) could exert a crucial effect on the development of human cancers, including CRC. However, the biological function and underlying mechanism of LINCRNA00460 in the development of CRC still need deeper exploration. Materials and methods: The expression of LINC00460 in CRC tissues and cell lines was assessed by qRT-PCR. Cell proliferation, migration, and invasion were measured by the respective cell counting Kit-8 (CCK-8), wound healing assay and transwell invasion assay. Cell apoptosis and caspase-3 activity were detected by flow cytometry and caspase-3 activity assay. The relationship between LINC00460 and miR-613 expression was explored by Dual-luciferase reporter assay. Protein expression was measured by Western blotting. In vivo tumour growth was evaluated using a xenograft model of nude mice. Results: LINC00460 was markedly up-regulated in CRC tissues and cell lines compared to their corresponding controls, which was closely correlated with clinical stage, TNM (T) classification, nodal (N) classification, metastasis (M) classification, liver metastasis and pathological differentiation, and survival rate of CRC patients. Functionally, LINC00460 knockdown decreased the proliferative, migrative and invasive abilities, and enhanced apoptosis rates and caspase-3 activity in HT29 and LOVO cells. Mechanistic studies indicated that miR-613 was targeted by LINC00460, and SphK1 was targeted and inversely regulated by miR-613 in HT29 and LOVO cells. In vivo studies, LINC00460 knockdown attenuated tumour growth. MiR-613 downregulation and SphK1 upregulation in the CRC tissues, and LINC00460 expression levels were inversely correlated with miR-613 expression and positively correlated with the SphK1 mRNA expression. Overall, LINC00460 modulated cell proliferation, migration, invasion and sphingosine kinase 1 (SphK1) expression in HT29 and LOVO cells, at least in most part, by regulating miR-613. Conclusion: LINC00460 functions as a competing endogenous RNA to regulate SphK1 expression by sponging miR-613 in CRC and provides a valuable therapeutic strategy for CRC patients. 

Retracted: No

PubPeer comments:
 Figure 6E and 6G. The results of cell invasion of LOVO cells co-transfected with pcDNA3.1+miR-613 mimics, and cell invasion of HT29 cells co-transfected with pcDNA3.1+si-LINC00460 seem to be from the same view. I think this is probably caused by the author misplaced the photos when composing. I hope the author could correct it as soon as possible. ![file] , 
 Published online 2021 Mar 30. doi: 10.2147 OTT.S302738 The authors have advised Figure 6E on page 7565 is incorrect. Due to an error at the time of figure assembly one of the images from 6G was used as a placeholder and not replaced later. The correct Figure 6 is shown below: ![file] ![file] The authors apologize for this error and advise it does not affect the results of the paper. ,