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Pathol Res Pract. 2018 Dec 26. pii: S0344-0338(18)31080-X. doi: 10.1016/j.prp.2018.12.031. [Epub ahead of print]

TCF3-activated LINC00152 exerts oncogenic role in osteosarcoma through regulating miR-1182/CDK14 axis.

Author information

1
Department of Orthopedics, The Second Affiliated Hospital of Suzhou University, Suzhou, Jiangsu, 215008, China; Department of Orthopedics, Chuzhou Medical College of Anhui Medical University, Chuzhou, Anhui, 239000, China.
2
Department of Intervention and Vascular Surgery, Shanghai Tenth People's Hospital Affiliated to Tongji University, Shanghai, 200000, China.
3
Department of Orthopedics, The Second Affiliated Hospital of Suzhou University, Suzhou, Jiangsu, 215008, China. Electronic address: Xiaozhong_Zhou20@163.com.

Abstract

Long noncoding RNAs (lncRNAs) have been reported to participate in tumorigenesis and diverse cellular processes in osteosarcoma (OS). However, the role of lncRNA LINC00152 in OS remains elusive. In this study, LINC00152 was highly expressed in osteosarcoma tissues and cell lines. Moreover, MTT and colony formation assays revealed that knockdown of LINC00152 significantly suppressed cell proliferation. The inhibitory effect of LINC00152 knockdown on OS cell migration and invasion was analyzed and demonstrated by transwell assays. Additionally, Chromatin immunoprecipitation (ChIP) and luciferase reporter assays suggested that LINC00152 was transcriptionally activated by the transcription factor TCF3. More importantly, mechanism investigation revealed that LINC00152 was predominantly located in the cytoplasm of OS cells and acted as a competing endogenous RNA (ceRNA) in OS by regulating miR-1182/CDK14 axis. Collectively, LINC00152 was activated by TCF3 and promotes cell proliferation and migration in osteosarcoma via miR-1182-CDK14 axis.

KEYWORDS:

CDK14; LINC00152; Osteosarcoma; TCF3; miR-1182

PMID:
30600185
DOI:
10.1016/j.prp.2018.12.031

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