SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway

doi:10.4251/wjgo.v16.i5.1890

科研成果详情

题名	SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway
作者	Jin, Xiao-Sheng; Chen, Lu-Xi; Ji, Ting-Ting; Li, Rong-Zhou
发表日期	2024
发表期刊	World Journal of Gastrointestinal Oncology; 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Cell cycle Colorectal cancer Phosphatidylinositol 3- kinase/AKT/mechanistic target of rapamycin Proliferation Serpin peptidase inhibitor clade H member 1
其他关键词	FATTY-ACID-METABOLISM ; SHOCK-PROTEIN 47 ; FOXO1
摘要	BACKGROUND Serpin peptidase inhibitor clade H member 1 (SERPINH1) was initially recognized as an oncogene implicated in various human malignancies. Nevertheless, the clinical relevance and functional implications of SERPINH1 in colorectal cancer (CRC) remain largely elusive. AIM To investigate the effects of SERPINH1 on CRC cells and its specific mechanism. METHODS Quantitative real-time polymerase chain reaction, western blotting analysis, The Cancer Genome Atlas data mining and immunohistochemistry were employed to examine SERPINH1 expression in CRC cell lines and tissues. A series of in-vitro assays were performed to demonstrate the function of SERPINH1 and its possible mechanisms in CRC. RESULTS SERPINH1 demonstrated elevated expression levels in both CRC cells and tissues, manifested at both mRNA and protein tiers. Elevated SERPINH1 levels correlated closely with advanced T stage, lymph node involvement, and distant metastasis, exhibiting a significant association with poorer overall survival among CRC patients. Subsequent investigations unveiled that SERPINH1 overexpression notably bolstered CRC cell proliferation, invasion, and migration in vitro, while conversely, SERPINH1 knockdown elicited the opposite effects. Gene set enrichment analysis underscored a correlation between SERPINH1 upregulation and genes associated with cell cycle regulation. Our findings underscored the capacity of heightened SERPINH1 levels to expedite G1/S phase cell cycle progression via phosphatidylinositol 3-kinase/AKT/mechanistic target of rapamycin pathway activation, thereby facilitating CRC cell invasion and migration. CONCLUSION These findings imply a crucial involvement of SERPINH1 in the advancement and escalation of CRC, potentially positioning it as a novel candidate for prognostic assessment and therapeutic intervention in CRC management.
资助项目	Ruian Natural Science Foundation [MS2021008]
出版者	BAISHIDENG PUBLISHING GROUP INC
ISSN	1948-5204
卷号	16 期号:5 页码:1890-1907
DOI	10.4251/wjgo.v16.i5.1890
页数	19
WOS类目	Oncology ; Gastroenterology & Hepatology
WOS研究方向	Oncology ; Gastroenterology & Hepatology
WOS记录号	WOS:001233475700012
收录类别	SCOPUS ; SCIE ; PUBMED
URL	查看原文
PubMed ID	38764814
SCOPUSEID	2-s2.0-85193703701
通讯作者地址	[Li, Rong-Zhou]Department of Gastroenterology,The Third Affiliated Hospital of Wenzhou Medical University,No. 108 Wansong Road, Zhejiang Province,Ruian,325000,China
Scopus学科分类	Oncology;Gastroenterology
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/213381
专题	其他_附属第三医院（瑞安市人民医院）
通讯作者	Li, Rong-Zhou
作者单位	Department of Gastroenterology,The Third Affiliated Hospital of Wenzhou Medical University,325000,China
第一作者单位	其他_附属第三医院（瑞安市人民医院）
通讯作者单位	其他_附属第三医院（瑞安市人民医院）
第一作者的第一单位	其他_附属第三医院（瑞安市人民医院）
推荐引用方式 GB/T 7714	Jin, Xiao-Sheng,Chen, Lu-Xi,Ji, Ting-Ting,et al. SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway[J]. World Journal of Gastrointestinal Oncology;,2024,16(5):1890-1907.
APA	Jin, Xiao-Sheng, Chen, Lu-Xi, Ji, Ting-Ting, & Li, Rong-Zhou. (2024). SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway. World Journal of Gastrointestinal Oncology;, 16(5), 1890-1907.
MLA	Jin, Xiao-Sheng,et al."SERPINH1 promoted the proliferation and metastasis of colorectal cancer by activating PI3K/Akt/mTOR signaling pathway".World Journal of Gastrointestinal Oncology; 16.5(2024):1890-1907.