中文版 | English
题名

Canopy FGF signaling regulator 3 affects prognosis, immune infiltration, and PI3K/AKT pathway in colon adenocarcinoma

作者
通讯作者Gao, Xu-Can
发表日期
2024-07-15
DOI
发表期刊
ISSN
1948-5204
卷号16期号:7
摘要
BACKGROUND Colon adenocarcinoma (COAD) is a malignant tumor of the digestive system. The mechanisms underlying COAD development and progression are still largely unknown. AIM To identify the role of canopy FGF signaling regulator 3 (CNPY3) in the development and progression of COAD by using bioinformatic tools and functional experiments. METHODS Bioinformatic data were downloaded from public databases. The associations of clinicopathological features, survival, and immune function with the expression of CNPY3 were analyzed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses and Gene Set Enrichment Analysis were used to explore the related pathways. Then, quantitative real-time PCR and immunohistochemistry were used for validation of CNPY3 expression in clinical samples and tumor cell lines. Cell lines with CNPY3 knockdown were constructed to further analyze gene functions. The functional experiments included proliferation, invasion, migration and apoptosis assays. RESULTS In both the TCGA cohort and the merged dataset, elevated CNPY3 expression was observed in tumor tissues. High CNPY3 expression correlated with adverse survival and compromised immune functions. Functional enrichment analysis suggested that the pro-oncogenic properties of CNPY3 might be linked to the PI3K-AKT signaling pathway. CNPY3 expression was validated at both the RNA and protein levels. Functional assays indicated that cell proliferation, invasion, and migration were inhibited and cell apoptosis was promoted after CNPY3 knockdown. Additionally, Western blot results revealed the downregulation of key proteins in the PI3K/AKT pathway following CNPY3 knockdown. PI3K/AKT pathway activator reversed the decrease in proliferation, invasion, and migration and the increase in apoptosis. Notably, CNPY3 knockdown still affected the cells when the pathway was inhibited. CONCLUSION This study showed that CNPY3 is upregulated in COAD and might regulate COAD development and progression by the PI3K/AKT pathway. Thus, CNPY3 might be a promising therapeutic target.
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收录类别
语种
英语
学校署名
第一 ; 通讯
WOS研究方向
Oncology ; Gastroenterology & Hepatology
WOS类目
Oncology ; Gastroenterology & Hepatology
WOS记录号
WOS:001281630600019
出版者
来源库
Web of Science
引用统计
被引频次[WOS]:1
成果类型期刊论文
条目标识符http://sustech.caswiz.com/handle/2SGJ60CL/790074
专题南方科技大学第一附属医院
作者单位
Southern Univ Sci & Technol, Shenzhen Peoples Hosp, Clin Med Coll 2, Affiliated Hosp 1,Dept Anorectal Surg,Jinan Univ, 1017 Dongmen North Rd,Cuizhu St, Shenzhen 518020, Guangdong, Peoples R China
第一作者单位南方科技大学第一附属医院
通讯作者单位南方科技大学第一附属医院
第一作者的第一单位南方科技大学第一附属医院
推荐引用方式
GB/T 7714
Gao, Xu-Can,Zhou, Biao-Huan,Ji, Zhou-Xin,et al. Canopy FGF signaling regulator 3 affects prognosis, immune infiltration, and PI3K/AKT pathway in colon adenocarcinoma[J]. WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY,2024,16(7).
APA
Gao, Xu-Can,Zhou, Biao-Huan,Ji, Zhou-Xin,Li, Qiang,&Liu, Hui-Ning.(2024).Canopy FGF signaling regulator 3 affects prognosis, immune infiltration, and PI3K/AKT pathway in colon adenocarcinoma.WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY,16(7).
MLA
Gao, Xu-Can,et al."Canopy FGF signaling regulator 3 affects prognosis, immune infiltration, and PI3K/AKT pathway in colon adenocarcinoma".WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY 16.7(2024).
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