Volume 15, Issue 12 pp. 1082-1091
RESEARCH ARTICLE

LINC00662 facilitates osteosarcoma progression via sponging miR-103a-3p and regulating SIK2 expression

Jianghu Huang

Jianghu Huang

Shengli Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China

Department of Orthopedics, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian, China

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Feiyue Lin

Feiyue Lin

Shengli Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China

Department of Orthopedics, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian, China

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Chuncai Xu

Chuncai Xu

Shengli Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China

Department of Orthopedics, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian, China

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Yang Xu

Corresponding Author

Yang Xu

Shengli Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China

Department of Orthopedics, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian, China

Correspondence

Yang Xu, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, 350001, Fujian, China; Department of Orthopedics, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, 350001, Fujian, China.

Email: [email protected]

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First published: 24 September 2021
Citations: 14

Jianghu Huang and Feiyue Lin are co-first authors.

Abstract

Long non-coding RNA (lncRNA) involvement in regulating assorted cancers has been determined. Long intergenic non-protein coding RNA 662 (LINC00662) has been studied in gastric cancer. However, its function was not elucidated in osteosarcoma (OS). Thus, we aimed to discover LINC00662 function and the corresponding mechanism in OS. In this study, we found that LINC00662 displayed high expression in OS cells. LINC00662 down-regulation negatively affected OS cell malignant behaviors and tumor growth. Subsequently, miR-103a-3p was proven to bind with LINC00662 and overexpression of miR-103a-3p inhibited OS cell proliferation, migration and invasion. Then, SIK2, the downstream of miR-103a-3p, was up-regulated in OS cells and positively regulated by LINC00662. In addition, knockdown of SIK2 exerted inhibitory effects on proliferative, migratory and invaded capacities of OS cells. More interestingly, miR-103a-3p depletion or SIK2 overexpression restored the impacts of down-regulated LINC00662 on OS cells. In conclusion, LINC00662 could facilitate OS progression via miR-103a-3p/SIK2 axis.

CONFLICT OF INTEREST

The authors declare that no conflict of interest exists in this study.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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