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.
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