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LINC01278 is Highly Expressed in Osteosarcoma and Participates in the Development of Tumors by Mediating the miR-134-5p/KRAS Axis

Authors Zhang GF, Zhou BS, An XC, An FM, Li SH

Received 1 June 2020

Accepted for publication 8 December 2020

Published 26 January 2021 Volume 2021:14 Pages 683—695

DOI https://doi.org/10.2147/OTT.S265591

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr XuYu Yang


Guo-Feng Zhang, Bai-Sui Zhou, Xiao-Chun An, Feng-Min An, Shan-Hui Li

Department of Orthopedics, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 261400, People’s Republic of China

Correspondence: Guo-Feng Zhang
Department of Orthopedics, Yantai Affiliated Hospital of Binzhou Medical University, No. 717, Jinbu Street, Yantai 264100, Shandong, People’s Republic of China
Tel +86-15905351140
Fax +86 535-4770841
Email gfzhangknu@gmail.com

Purpose: There is increasing evidence that non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), produce a critical regulatory effect on osteosarcoma (OS). LINC01278, as a newly discovered lncRNA, is found to be highly expressed in OS, but its related mechanism remains unclear. This research, therefore, is designed to study the mechanism of LINC01278 in OS and to find potential targets for clinical use.
Methods: qRT-PCR was applied to determine the relative expression of LINC01278 and analyze its diagnostic value in OS. CCK-8, Transwell and flow cytometry were utilized for the determination of cell proliferation, migration/invasion, and apoptosis. RIP and RNA pull-down experiments were used to verify the targeted binding effect of miR-134-5p and LINC01278. The relationship between miR-134-5p and LINC01278 or KRAS was analyzed using dual luciferase reporter gene. The effects of LINC01278 on tumor growth in nude mice was analyzed by in vivo experiment.
Results: qRT-PCR showed that LINC01278 increased in OS tissues and serum, indicating poor prognosis. In addition, LINC01278 was also of high value for OS diagnosis. Functional experiments showed that LINC01278 inhibited KRAS-mediated OS cell proliferation and metastasis through miR-134-5p. Finally, the results of an in vivo animal model indicated that LINC01278 promoted OS growth.
Conclusion: LINC01278 is expressed highly in OS, and patients with high LINC01278 expression have poor prognosis. Moreover, LINC01278 can suppress the proliferation and apoptosis of OS cells through mediating miR-134-5p/KRAS axis, which is expected to become a potential therapeutic target for OS.

Keywords: LINC01278, miR-134-5p, KRAS, osteosarcoma, proliferation, apoptosis

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