Publication Name	World Journal of Gastrointestinal Oncology
Manuscript ID	89309
Country	China

Category	Biochemistry & Molecular Biology
Manuscript Type	Basic Study
Article Title	Complement factor I knockdown inhibits colon cancer development by affecting Wnt/β-catenin/c-Myc signaling pathway and glycolysis
Manuscript Source	Unsolicited Manuscript
All Author List	Yong-Jun Du, Yue Jiang, Yan-Mei Hou and Yong-Bo Shi
Funding Agency and Grant Number
Corresponding Author	Yong-Bo Shi, MM, Associate Chief Physician, Department of Proctology, Zigong Hospital of Traditional Chinese Medicine, No. 59 Machongkou Street, Da’an District, Zigong 643000, Sichuan Province, China. syb821004@163.com
Key Words	Colon cancer; Immune infiltration; Complement factor I; Glycolysis; Wnt/β-catenin/c-Myc pathway
Core Tip	We identified six hub immune infiltration-related differentially expressed genes, of which the expression of complement factor I (CFI), complement factor B, lymphoid enhancer binding factor 1, and SRY-related high-mobility-group box 4 were upregulated, whereas that of fatty acid-binding protein 1 and bone morphogenic protein-2 were downregulated. CFI knockdown inhibited HT29 and HCT116 cell proliferation, migration, invasion, and tumor growth in a colon cancer (CC) mouse model constructed from HT29 cells. CFI knockdown suppressed the expression of glycolysis-related proteins (glucose transporter type 1, hexokinase 2, lactate dehydrogenase A, and pyruvate kinase M2) and Wnt/β-catenin/c-Myc-related protein-expression levels (β-catenin and c-Myc). CFI knockdown suppressed glycolysis by inhibiting the Wnt/β-catenin/c-Myc signaling pathway. These findings delineate a potential therapeutic strategy for the clinical management of CC.
Citation	Du YJ, Jiang Y, Hou YM, Shi YB. Complement factor I knockdown inhibits colon cancer development by affecting Wnt/β-catenin/c-Myc signaling pathway and glycolysis. World J Gastrointest Oncol 2024; In press

Received	2023-10-27 07:05
Peer-Review Started	2023-10-27 07:06
To Make the First Decision
Return for Revision	2024-01-06 07:17
Revised	2024-01-24 08:05
Second Decision	2024-03-27 02:35
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief	2024-03-27 04:53
Articles in Press	2024-03-27 04:53
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ISSN	1948-5204 (online)
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