Tumor necrosis factor promotes doublecortin-like kinase 1 expression and cellular reprogramming in intestinal epithelial cells leading to neoplastic transformation

Background Tumor necrosis factor (TNF) is a critical mediator in chronic inflammation and colorectal cancer (CRC) progression. However, whether and how prolonged TNF exposure triggers CRC is not fully understood. Methods TNF-induced expression of Dclk1 , a cancer stem cell (CSC) marker, was assessed...

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Bibliographic Details
Published in:	Cell communication and signaling Vol. 23; no. 1; pp. 415 - 19
Main Authors:	Huang, Lin, Li, Tianqi, Huang, Xu, Chen, Xiaoxi, Ju, Yuanyuan, Xu, Lili, Ma, Chunhua, Tao, Yumei, Yang, Yonghong, Bian, Xiaoyun, Huycke, Mark M., Wang, Xingmin
Format:	Journal Article
Language:	English
Published:	London BioMed Central 02.10.2025 BioMed Central Ltd Springer Nature B.V BMC
Subjects:	Analysis Animal models Antimitotic agents Antineoplastic agents Biomedical and Life Sciences c-Myc protein Cancer Cancer therapies Cell activation Cell Biology Cell culture Cell State and Fate in Health and Disease Colitis Colorectal cancer Colorectal cancer stem cells Colorectal carcinoma Complications and side effects Cytokines Cytokines and Growth Factors Development and progression Doublecortin protein Doublecortin-like kinase 1 EMT Epithelial cells Gene expression Genetic aspects Genetic engineering Genetic transformation Health aspects Immunodeficiency Inflammation Inflammatory bowel disease Intestine Kinases Life Sciences Medical prognosis Myc protein Necrosis NF-κB protein Oncology, Experimental Organoid Organoids Penicillin G Protein-Ligand Interactions Receptors Reprogramming RNA RNA sequencing Stem cells Therapeutic targets TNF-humanized mice Transcription factors Transgenic animals Transgenic mice Tumor necrosis factor Tumor necrosis factor-TNF Tumorigenesis Tumors Xenografts China Shanghai China TNF-humanized mice Organoid Reprogramming Doublecortin-like kinase 1 EMT Colorectal cancer stem cells
ISSN:	1478-811X, 1478-811X
Online Access:	Get full text
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