SUMO-specific protease 2 (SENP2) functions as a tumor suppressor in osteosarcoma via SOX9 degradation

Osteosarcoma (OS) is the most common primary bone malignancy in children and adolescents, the pathogenesis of which remain largely unknown. Small ubiquitin-like modifier (SUMO)-Specific Protease 2 (SENP2) has been reported to serve as a tumor suppressor in hepatocellular carcinoma cells. The aim of...

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Published inExperimental and therapeutic medicine Vol. 16; no. 6; pp. 5359 - 5365
Main Authors Pei, Hong, Chen, Liang, Liao, Quan-Ming, Wang, Ke-Jun, Chen, Shun-Guang, Liu, Zheng-Jie, Zhang, Zhi-Cai
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.12.2018
Spandidos Publications UK Ltd
D.A. Spandidos
Subjects
Biotechnology
Bone cancer
Cancer
Carcinoma
Cell growth
Cell migration
Cell proliferation
CRISPR
Genes
Genetic aspects
Genome editing
Hepatocellular carcinoma
Operating systems (Software)
Osteosarcoma
Plasmids
Polymerase chain reaction
Proteases
Proteins
Sarcoma
Sumo
Tumors
Ubiquitin
Youth
United States > US
China
Germany
small ubiquitin-like modifier-specific protease 2
SRY-box-9
degradation
osteosarcoma
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Summary:Osteosarcoma (OS) is the most common primary bone malignancy in children and adolescents, the pathogenesis of which remain largely unknown. Small ubiquitin-like modifier (SUMO)-Specific Protease 2 (SENP2) has been reported to serve as a tumor suppressor in hepatocellular carcinoma cells. The aim of the present study was to investigate the critical role of SENP2 in OS cells. Using reverse transcription-quantitative polymerase chain reaction and western blot assays, it was observed that SENP2 was significantly downregulated in clinical OS tissues compared with adjacent normal samples. Ectopic expression of SENP2 resulted in the suppression of proliferation, migration and invasion in OS cells, whereas SENP2 knockdown by CRISPR-Cas9-based gene editing had the opposite effect. SENP2 is associated with the proteasome-dependent ubiquitination and degradation of SRY-box-9 (SOX9). SOX9 silencing impaired SENP2-depletion-induced accelerated cell growth and migration. Together, these results suggest that SOX9 is a critical downstream effector of the tumor suppressor SENP2 in OS.
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ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2018.6838