SUMO-specific protease 6 promotes gastric cancer cell growth via deSUMOylation of FoxM1

SUMOylation is a post-translational modification exerted various effects on the target proteins. SUMOylation is a highly dynamic and reversible process, which has been shown to play an important role in tumorigenesis. However, the roles of sentrin/SUMO-specific proteases (SENPs), which mediate the r...

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Bibliographic Details
Published inTumor biology Vol. 36; no. 12; pp. 9865 - 9871
Main Authors Song, Jiu-Gang, Xie, Hua-Hong, Li, Nan, Wu, Kai, Qiu, Ji-Gang, Shen, Da-Ming, Huang, Chun-Jin
Format Journal Article
LanguageEnglish
Published United States Springer Nature B.V 01.12.2015
Subjects
Cancer
Carcinogenesis - genetics
Cell Line, Tumor
Cell Proliferation - genetics
Cysteine Endopeptidases - biosynthesis
Cysteine Endopeptidases - genetics
Forkhead Box Protein M1
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Gastrointestinal diseases
Gene Expression Regulation, Neoplastic
Humans
Proteases
Protein Processing, Post-Translational - genetics
RNA, Messenger - biosynthesis
Stomach Neoplasms - genetics
Stomach Neoplasms - pathology
Sumoylation - genetics
SENP6
Cell growth
SUMOylation
FoxM1
Gastric cancer
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Summary:SUMOylation is a post-translational modification exerted various effects on the target proteins. SUMOylation is a highly dynamic and reversible process, which has been shown to play an important role in tumorigenesis. However, the roles of sentrin/SUMO-specific proteases (SENPs), which mediate the reverse process of SUMOylation, in tumorigenesis remains largely unexplored. Here, we uncover a critical role of SENP6 in promoting gastric cancer cells growth via regulating the deSUMOylation of a transcription factor forkhead box protein M1 (FoxM1). We demonstrated that the mRNA and protein levels were elevated in gastric cancer tissues. Overexpression of SENP6 promoted, while RNA interference depletion of endogenous SENP6 inhibited gastric cancer cells growth and the ability of colony formation. By using biochemical assays, we identified FoxM1 as a novel substrate of SENP6 in gastric cancer cells. Thus, our data suggest that SENP6, which is highly expressed in gastric cancer cells, regulates the transcriptional activity and stability of FoxM1 through deSUMOylation.
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ISSN:1010-4283
1423-0380
DOI:10.1007/s13277-015-3737-z