잠시만 기다려 주세요. 로딩중입니다.

LncRNA LINC00313 Knockdown Inhibits Tumorigenesis and Metastasis in Human Osteosarcoma by Upregulating FOSL2 through Sponging miR-342-3p

Yonsei Medical Journal 2020년 61권 5호 p.359 ~ 370
Chen Hongtao, Wahafu Paerhati, Wang Leilei, Chen Xuan,
소속 상세정보
 ( Chen Hongtao ) - Xinjiang Medical University Sixth Affiliated Hospital Department of Orthopedics
 ( Wahafu Paerhati ) - Xinjiang Medical University Sixth Affiliated Hospital Department of Orthopedics
 ( Wang Leilei ) - Xinjiang Medical University Sixth Affiliated Hospital Department of Orthopedics
 ( Chen Xuan ) - Xinjiang Medical University Sixth Affiliated Hospital Department of Orthopedics

Abstract


Purpose: Osteosarcoma (OS) is the most common primary bone tumor, with high morbidity in infants and adolescents. Long noncoding RNA LINC00313 has been found to modulate papillary thyroid cancer tumorigenesis and to be dysregulate in lung cancer. However, the role of LINC00313 in OS has not yet been addressed.

Materials and Methods: We evaluated mRNA and protein expression using real-time quantitative PCR and Western blotting. Cell proliferation was evaluated using MTT; apoptosis and autophagy were assessed with flow cytometry, Western blotting, and/or GFP-LC3 assay. Transwell assay was conducted to measure cell migration and invasion. Potential target sites for LINC00313 and miR-342-3p were predicted with starBase v.2.0 and TargetScan Human, and verified using luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay. In vivo, xenogeneic tumors were induced with U2OS and MG-63 cells, separately.

Results: LINC00313 was upregulated and miR-342-3p was downregulated in OS tissues and cells. High expression of LINC00313 was associated with shorter overall survival. FOSL2 downregulation and miR-342-3p overexpression suppressed cell proliferation and migratory and invasive abilities while promoting apoptosis and autophagy, all of which were consistent with the effects of LINC00313 knockdown. miR-342-3p, sponged by LINC00313, inversely modulated FOSL2 by targeting MG-63 cells, and FOSL2 expression was positively controlled by LINC00313. LINC00313 knockdown suppressed tumor growth in vivo.

Conclusion: LINC00313 is upregulated in OS, and LINC00313 knockdown plays a vital anti-tumor role in OS cell progression through a miR-342-3p/FOSL2 axis. Our study suggests that LINC00313 may be a novel, promising biomarker for diagnosis and prognosis of OS.

키워드

LINC00313; miR-342-3p; FOSL2; osteosarcoma (OS)

원문 및 링크아웃 정보

  

등재저널 정보