SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30

Abstract Background Splicing factor SRSF3 is an oncogene and overexpressed in various kinds of cancers, however, the function and mechanism involved in colorectal cancer (CRC) remained unclear. The aim of this study was to explore the relationship between SRSF3 and carcinogenesis and progression of...

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Main Authors: Ji-Lin Wang, Chun-Rong Guo, Tian-Tian Sun, Wen-Yu Su, Qiang Hu, Fang-Fang Guo, Lun-Xi Liang, Jie Xu, Hua Xiong, Jing-Yuan Fang
Format: Article
Language:English
Published: BMC 2020-04-01
Series:Cancer Cell International
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12935-020-01201-2
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author Ji-Lin Wang
Chun-Rong Guo
Tian-Tian Sun
Wen-Yu Su
Qiang Hu
Fang-Fang Guo
Lun-Xi Liang
Jie Xu
Hua Xiong
Jing-Yuan Fang
author_facet Ji-Lin Wang
Chun-Rong Guo
Tian-Tian Sun
Wen-Yu Su
Qiang Hu
Fang-Fang Guo
Lun-Xi Liang
Jie Xu
Hua Xiong
Jing-Yuan Fang
author_sort Ji-Lin Wang
collection DOAJ
description Abstract Background Splicing factor SRSF3 is an oncogene and overexpressed in various kinds of cancers, however, the function and mechanism involved in colorectal cancer (CRC) remained unclear. The aim of this study was to explore the relationship between SRSF3 and carcinogenesis and progression of CRC. Methods The expression of SRSF3 in CRC tissues was detected by immunohistochemistry. The proliferation and invasion rate was analyzed by CCK-8 assay, colony formation assay, transwell invasion assay and xenograft experiment. The expression of selected genes was detected by western blot or real time PCR. Results SRSF3 is overexpressed in CRC tissues and its high expression was associated with CRC differentiation, lymph node invasion and AJCC stage. Upregulation of SRSF3 was also associated with shorter overall survival. Knockdown of SRSF3 in CRC cells activated ArhGAP30/Ace-p53 and decreased cell proliferation, migration and survival; while ectopic expression of SRSF3 attenuated ArhGAP30/Ace-p53 and increases cell proliferation, migration and survival. Targeting SRSF3 in xenograft tumors suppressed tumor progression in vivo. Conclusions Taken together, our data identify SRSF3 as a regulator for ArhGAP30/Ace-p53 in CRC, and highlight potential prognostic and therapeutic significance of SRSF3 in CRC.
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spelling doaj.art-b33c45ae4ccb4145965478d540b562ed2022-12-21T22:31:38ZengBMCCancer Cell International1475-28672020-04-012011910.1186/s12935-020-01201-2SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30Ji-Lin Wang0Chun-Rong Guo1Tian-Tian Sun2Wen-Yu Su3Qiang Hu4Fang-Fang Guo5Lun-Xi Liang6Jie Xu7Hua Xiong8Jing-Yuan Fang9Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityThe Centre of Teaching and Experiment, Shanghai University of Traditional Chinese MedicineDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityDivision of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong UniversityAbstract Background Splicing factor SRSF3 is an oncogene and overexpressed in various kinds of cancers, however, the function and mechanism involved in colorectal cancer (CRC) remained unclear. The aim of this study was to explore the relationship between SRSF3 and carcinogenesis and progression of CRC. Methods The expression of SRSF3 in CRC tissues was detected by immunohistochemistry. The proliferation and invasion rate was analyzed by CCK-8 assay, colony formation assay, transwell invasion assay and xenograft experiment. The expression of selected genes was detected by western blot or real time PCR. Results SRSF3 is overexpressed in CRC tissues and its high expression was associated with CRC differentiation, lymph node invasion and AJCC stage. Upregulation of SRSF3 was also associated with shorter overall survival. Knockdown of SRSF3 in CRC cells activated ArhGAP30/Ace-p53 and decreased cell proliferation, migration and survival; while ectopic expression of SRSF3 attenuated ArhGAP30/Ace-p53 and increases cell proliferation, migration and survival. Targeting SRSF3 in xenograft tumors suppressed tumor progression in vivo. Conclusions Taken together, our data identify SRSF3 as a regulator for ArhGAP30/Ace-p53 in CRC, and highlight potential prognostic and therapeutic significance of SRSF3 in CRC.http://link.springer.com/article/10.1186/s12935-020-01201-2SRSF3ArhGAP30Colorectal cancer
spellingShingle Ji-Lin Wang
Chun-Rong Guo
Tian-Tian Sun
Wen-Yu Su
Qiang Hu
Fang-Fang Guo
Lun-Xi Liang
Jie Xu
Hua Xiong
Jing-Yuan Fang
SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30
Cancer Cell International
SRSF3
ArhGAP30
Colorectal cancer
title SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30
title_full SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30
title_fullStr SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30
title_full_unstemmed SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30
title_short SRSF3 functions as an oncogene in colorectal cancer by regulating the expression of ArhGAP30
title_sort srsf3 functions as an oncogene in colorectal cancer by regulating the expression of arhgap30
topic SRSF3
ArhGAP30
Colorectal cancer
url http://link.springer.com/article/10.1186/s12935-020-01201-2
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