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LINC01224 Promotes Colorectal Cancer Progression by Sponging miR-2467

Authors Chen L, Chen W, Zhao C, Jiang Q

Received 12 September 2020

Accepted for publication 31 December 2020

Published 26 January 2021 Volume 2021:13 Pages 733—742


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Antonella D'Anneo

Lin Chen,1 Wei Chen,1 Changjie Zhao,2 Qi Jiang1

1Department of Gastroenterology, Affiliated Dongtai Hospital of Nantong University, Dongtai, Jiangsu 224200, People’s Republic of China; 2Endoscopy Center, Affiliated Dongtai Hospital of Nantong University, Dongtai, Jiangsu 224200, People’s Republic of China

Correspondence: Qi Jiang
Department of Gastroenterology, Affiliated Dongtai Hospital of Nantong University, 2 Kangfuxi Road, Dongtai, Jiangsu 224200, People’s Republic of China

Introduction: Colorectal cancer (CRC) is one of the most common human cancers and a leading cause of cancer-related death. Accumulating evidence has confirmed that long non-coding RNA (lncRNA) plays crucial roles in CRC development.
Methods: qRT-PCR was performed to examine the expressions of LINC01224 and miR-2467. CCK-8 assay, colony formation assay and transwell invasion assay were used to examine the progression of breast cancer cells. Luciferase and RNA-binding protein immunoprecipitation (RIP) assay were applied to verify the binding site. Correlation analysis of miR-2467 and LINC01224 expression in lung cancer tissues was shown. Pancreatic cancer cells growth in vivo was evaluated using xenograft tumor assay.
Results: LINC01224 expression was observed to be up-regulated in CRC tissues and cell lines. Functional studies suggested that LINC01224 silence inhibited CRC cells proliferation and invasion of CRC cells, while co-transfection with a miR-2467 inhibitor reversed these biological effects. Luciferase reporter assays illustrated that LINC01224 regulated miR-2467 directly, and RNA-binding protein immunoprecipitation (RIP) further confirmed that the suppression of LINC01224 by miR-2467 was in an RISC-dependent manner. Finally, LINC01224 silence inhibited the growth CRC cells in vivo.
Conclusion: In conclusion, our findings showed that LINC01224 promoted CRC progression through sponging miR-2467. LINC01224 may serve as a potential diagnostic biomarker and therapeutic target for CRC patients.

Keywords: LINC01224, miR-2467, colorectal cancer, proliferation, invasion

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