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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| Veröffentlicht in: | Cell communication and signaling Jg. 23; H. 1; S. 415 - 19 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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London
BioMed Central
02.10.2025
BioMed Central Ltd Springer Nature B.V BMC |
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| Abstract | 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 in IEC-6 intestinal epithelial cells, murine models, and colon organoids. TNF-induced reprogramming of intestinal epithelial cells was investigated through single-cell RNA sequencing and cellular transformation assayed by xenograft tumor model.
Results
We observed a significant increase in Dclk1 in the intestines of
TNF
-transgenic mice and TNF-treated IEC-6 cells. Notably,
DCLK1
expression correlated positively with inflammation, TNF levels, and TNFRSF1a in human subjects. Silencing of
Tnfrsf1a
markedly reduced
Dclk1
expression, underscoring the role of TNF-Tnfrsf1a axis in the regulation of
Dclk1
expression. Furthermore, Dclk1-positive cells were significantly elevated in the intestines of TNF-treated wild-type mice, but not in
Tnfrsf1a
−/−
mice, compared to controls. Inhibition of NFκB and c-Myc also led to a marked reduction in
Dclk1
expression. Intriguingly, colonic organoids derived from
TNF
-transgenic mice exhibited increased numbers and sizes, whereas those from
Tnfrsf1a
−/−
mice showed the opposite trend. Single-cell RNA sequencing revealed that prolonged TNF exposure induced CSC emergence through the reprogramming of Dclk1-positive tuft cells and activation of CRC-related pathways. Critically, prolonged TNF treatment resulted in neoplastic transformation of intestinal epithelial cells, leading to xenograft tumor formation in immunodeficient mice.
Conclusions
These findings provide novel insights into how chronic inflammation drives the genesis of intestinal CSCs and fosters CRC development, highlighting potential therapeutic targets for combating colitis-associated colorectal cancer. |
|---|---|
| AbstractList | 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 in IEC-6 intestinal epithelial cells, murine models, and colon organoids. TNF-induced reprogramming of intestinal epithelial cells was investigated through single-cell RNA sequencing and cellular transformation assayed by xenograft tumor model. Results We observed a significant increase in Dclk1 in the intestines of TNF-transgenic mice and TNF-treated IEC-6 cells. Notably, DCLK1 expression correlated positively with inflammation, TNF levels, and TNFRSF1a in human subjects. Silencing of Tnfrsf1a markedly reduced Dclk1 expression, underscoring the role of TNF-Tnfrsf1a axis in the regulation of Dclk1 expression. Furthermore, Dclk1-positive cells were significantly elevated in the intestines of TNF-treated wild-type mice, but not in Tnfrsf1a.sup.-/- mice, compared to controls. Inhibition of NFκB and c-Myc also led to a marked reduction in Dclk1 expression. Intriguingly, colonic organoids derived from TNF-transgenic mice exhibited increased numbers and sizes, whereas those from Tnfrsf1a.sup.-/- mice showed the opposite trend. Single-cell RNA sequencing revealed that prolonged TNF exposure induced CSC emergence through the reprogramming of Dclk1-positive tuft cells and activation of CRC-related pathways. Critically, prolonged TNF treatment resulted in neoplastic transformation of intestinal epithelial cells, leading to xenograft tumor formation in immunodeficient mice. Conclusions These findings provide novel insights into how chronic inflammation drives the genesis of intestinal CSCs and fosters CRC development, highlighting potential therapeutic targets for combating colitis-associated colorectal cancer. Keywords: Colorectal cancer stem cells, TNF-humanized mice, Doublecortin-like kinase 1, Organoid, Reprogramming, EMT Section BackgroundTumor 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.AbstractSection MethodsTNF-induced expression of Dclk1, a cancer stem cell (CSC) marker, was assessed in IEC-6 intestinal epithelial cells, murine models, and colon organoids. TNF-induced reprogramming of intestinal epithelial cells was investigated through single-cell RNA sequencing and cellular transformation assayed by xenograft tumor model.AbstractSection ResultsWe observed a significant increase in Dclk1 in the intestines of TNF-transgenic mice and TNF-treated IEC-6 cells. Notably, DCLK1 expression correlated positively with inflammation, TNF levels, and TNFRSF1a in human subjects. Silencing of Tnfrsf1a markedly reduced Dclk1 expression, underscoring the role of TNF-Tnfrsf1a axis in the regulation of Dclk1 expression. Furthermore, Dclk1-positive cells were significantly elevated in the intestines of TNF-treated wild-type mice, but not in Tnfrsf1a−/− mice, compared to controls. Inhibition of NFκB and c-Myc also led to a marked reduction in Dclk1 expression. Intriguingly, colonic organoids derived from TNF-transgenic mice exhibited increased numbers and sizes, whereas those from Tnfrsf1a−/− mice showed the opposite trend. Single-cell RNA sequencing revealed that prolonged TNF exposure induced CSC emergence through the reprogramming of Dclk1-positive tuft cells and activation of CRC-related pathways. Critically, prolonged TNF treatment resulted in neoplastic transformation of intestinal epithelial cells, leading to xenograft tumor formation in immunodeficient mice.AbstractSection ConclusionsThese findings provide novel insights into how chronic inflammation drives the genesis of intestinal CSCs and fosters CRC development, highlighting potential therapeutic targets for combating colitis-associated colorectal cancer. 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. TNF-induced expression of Dclk1, a cancer stem cell (CSC) marker, was assessed in IEC-6 intestinal epithelial cells, murine models, and colon organoids. TNF-induced reprogramming of intestinal epithelial cells was investigated through single-cell RNA sequencing and cellular transformation assayed by xenograft tumor model. We observed a significant increase in Dclk1 in the intestines of TNF-transgenic mice and TNF-treated IEC-6 cells. Notably, DCLK1 expression correlated positively with inflammation, TNF levels, and TNFRSF1a in human subjects. Silencing of Tnfrsf1a markedly reduced Dclk1 expression, underscoring the role of TNF-Tnfrsf1a axis in the regulation of Dclk1 expression. Furthermore, Dclk1-positive cells were significantly elevated in the intestines of TNF-treated wild-type mice, but not in Tnfrsf1a.sup.-/- mice, compared to controls. Inhibition of NFκB and c-Myc also led to a marked reduction in Dclk1 expression. Intriguingly, colonic organoids derived from TNF-transgenic mice exhibited increased numbers and sizes, whereas those from Tnfrsf1a.sup.-/- mice showed the opposite trend. Single-cell RNA sequencing revealed that prolonged TNF exposure induced CSC emergence through the reprogramming of Dclk1-positive tuft cells and activation of CRC-related pathways. Critically, prolonged TNF treatment resulted in neoplastic transformation of intestinal epithelial cells, leading to xenograft tumor formation in immunodeficient mice. These findings provide novel insights into how chronic inflammation drives the genesis of intestinal CSCs and fosters CRC development, highlighting potential therapeutic targets for combating colitis-associated colorectal cancer. 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 in IEC-6 intestinal epithelial cells, murine models, and colon organoids. TNF-induced reprogramming of intestinal epithelial cells was investigated through single-cell RNA sequencing and cellular transformation assayed by xenograft tumor model. Results We observed a significant increase in Dclk1 in the intestines of TNF -transgenic mice and TNF-treated IEC-6 cells. Notably, DCLK1 expression correlated positively with inflammation, TNF levels, and TNFRSF1a in human subjects. Silencing of Tnfrsf1a markedly reduced Dclk1 expression, underscoring the role of TNF-Tnfrsf1a axis in the regulation of Dclk1 expression. Furthermore, Dclk1-positive cells were significantly elevated in the intestines of TNF-treated wild-type mice, but not in Tnfrsf1a −/− mice, compared to controls. Inhibition of NFκB and c-Myc also led to a marked reduction in Dclk1 expression. Intriguingly, colonic organoids derived from TNF -transgenic mice exhibited increased numbers and sizes, whereas those from Tnfrsf1a −/− mice showed the opposite trend. Single-cell RNA sequencing revealed that prolonged TNF exposure induced CSC emergence through the reprogramming of Dclk1-positive tuft cells and activation of CRC-related pathways. Critically, prolonged TNF treatment resulted in neoplastic transformation of intestinal epithelial cells, leading to xenograft tumor formation in immunodeficient mice. Conclusions These findings provide novel insights into how chronic inflammation drives the genesis of intestinal CSCs and fosters CRC development, highlighting potential therapeutic targets for combating colitis-associated colorectal cancer. Abstract 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 in IEC-6 intestinal epithelial cells, murine models, and colon organoids. TNF-induced reprogramming of intestinal epithelial cells was investigated through single-cell RNA sequencing and cellular transformation assayed by xenograft tumor model. Results We observed a significant increase in Dclk1 in the intestines of TNF-transgenic mice and TNF-treated IEC-6 cells. Notably, DCLK1 expression correlated positively with inflammation, TNF levels, and TNFRSF1a in human subjects. Silencing of Tnfrsf1a markedly reduced Dclk1 expression, underscoring the role of TNF-Tnfrsf1a axis in the regulation of Dclk1 expression. Furthermore, Dclk1-positive cells were significantly elevated in the intestines of TNF-treated wild-type mice, but not in Tnfrsf1a −/− mice, compared to controls. Inhibition of NFκB and c-Myc also led to a marked reduction in Dclk1 expression. Intriguingly, colonic organoids derived from TNF-transgenic mice exhibited increased numbers and sizes, whereas those from Tnfrsf1a −/− mice showed the opposite trend. Single-cell RNA sequencing revealed that prolonged TNF exposure induced CSC emergence through the reprogramming of Dclk1-positive tuft cells and activation of CRC-related pathways. Critically, prolonged TNF treatment resulted in neoplastic transformation of intestinal epithelial cells, leading to xenograft tumor formation in immunodeficient mice. Conclusions These findings provide novel insights into how chronic inflammation drives the genesis of intestinal CSCs and fosters CRC development, highlighting potential therapeutic targets for combating colitis-associated colorectal cancer. |
| ArticleNumber | 415 |
| Audience | Academic |
| Author | Yang, Yonghong Chen, Xiaoxi Wang, Xingmin Huang, Xu Bian, Xiaoyun Huycke, Mark M. Xu, Lili Ju, Yuanyuan Ma, Chunhua Huang, Lin Tao, Yumei Li, Tianqi |
| Author_xml | – sequence: 1 givenname: Lin surname: Huang fullname: Huang, Lin organization: Department of Gastroenterology, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Key Laboratory of Genetics and Reproductive Medicine – sequence: 2 givenname: Tianqi surname: Li fullname: Li, Tianqi organization: Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Key Laboratory of Genetics and Reproductive Medicine – sequence: 3 givenname: Xu surname: Huang fullname: Huang, Xu organization: Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Key Laboratory of Genetics and Reproductive Medicine – sequence: 4 givenname: Xiaoxi surname: Chen fullname: Chen, Xiaoxi organization: Department of Gastroenterology, Affiliated Maternity and Child Healthcare Hospital of Nantong University – sequence: 5 givenname: Yuanyuan surname: Ju fullname: Ju, Yuanyuan organization: Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Key Laboratory of Genetics and Reproductive Medicine – sequence: 6 givenname: Lili surname: Xu fullname: Xu, Lili organization: Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Key Laboratory of Genetics and Reproductive Medicine – sequence: 7 givenname: Chunhua surname: Ma fullname: Ma, Chunhua organization: Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Key Laboratory of Genetics and Reproductive Medicine – sequence: 8 givenname: Yumei surname: Tao fullname: Tao, Yumei organization: Department of Pathology, Affiliated Maternity and Child Healthcare Hospital of Nantong University – sequence: 9 givenname: Yonghong surname: Yang fullname: Yang, Yonghong organization: Department of Nephrology, Rheumatology, and Immunology, Nantong Children’s Hospital – sequence: 10 givenname: Xiaoyun surname: Bian fullname: Bian, Xiaoyun organization: Department of Gastroenterology, Affiliated Maternity and Child Healthcare Hospital of Nantong University – sequence: 11 givenname: Mark M. surname: Huycke fullname: Huycke, Mark M. organization: Department of Radiation Oncology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center – sequence: 12 givenname: Xingmin surname: Wang fullname: Wang, Xingmin email: xingmin-wang@ntu.edu.cn organization: Nantong Institute of Genetics and Reproductive Medicine, Affiliated Maternity and Child Healthcare Hospital of Nantong University, Nantong Key Laboratory of Genetics and Reproductive Medicine, Nantong Maternity and Child Healthcare Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/41039610$$D View this record in MEDLINE/PubMed |
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Tumor necrosis factor (TNF) is a critical mediator in chronic inflammation and colorectal cancer (CRC) progression. However, whether and how... Tumor necrosis factor (TNF) is a critical mediator in chronic inflammation and colorectal cancer (CRC) progression. However, whether and how prolonged TNF... Background Tumor necrosis factor (TNF) is a critical mediator in chronic inflammation and colorectal cancer (CRC) progression. However, whether and how... Section BackgroundTumor necrosis factor (TNF) is a critical mediator in chronic inflammation and colorectal cancer (CRC) progression. However, whether and how... Abstract Background Tumor necrosis factor (TNF) is a critical mediator in chronic inflammation and colorectal cancer (CRC) progression. However, whether and... |
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