IL-13/IL-13RA2 signaling promotes colorectal cancer stem cell tumorigenesis by inducing ubiquitinated degradation of p53

He, Bin; Ji, Liang; Qin, Qianqian; Zhang, Yuqin; Shi, Shuo; Cao, Jianyu; Zhang, Zhixin; Bie, Qingli; Zhao, Rou; Wei, Li; Zhang, Baogui; Zhang, Bin

doi:10.1016/j.gendis.2023.01.027

Cited by 14 publications

(6 citation statements)

References 41 publications

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“…The ubiquitin–proteasome system (UPS) is the most important mechanism for p53 degradation (Allende-Vega and Saville 2010 ). IL-13/IL-13RA2 signalling promotes stemness, proliferation and invasive migration in colorectal cancer by inducing p53 ubiquitination degradation (He et al 2024 ).Therefore, we hypothesized that the autophagy activation induced by MARCH5 might be mediated by p53 ubiquitination. Our results essentially confirm that MARCH5 stimulation promotes p53 ubiquitination.…”

Section: Discussionmentioning

confidence: 95%

MARCH5 promotes hepatocellular carcinoma progression by inducing p53 ubiquitination degradation

Cai,

Gao,

Yan

et al. 2024

J Cancer Res Clin Oncol

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Background Human MARCH5 is a mitochondria-localized E3 ubiquitin-protein ligase that is essential for the regulation of mitochondrial dynamics. A large body of evidence suggests that imbalances in mitochondrial dynamics are strongly associated with cancer. However, the expression, biological function and prognostic significance of MARCH5 in hepatocellular carcinoma (HCC) have not been determined. Materials and methods The mRNA and protein expression of MARCH5 in HCC cell lines and tumor tissues was assessed by real-time quantitative PCR, Western blot analysis and immunohistochemistry. The clinical prognostic significance of MARCH5 was evaluated in 135 HCC patients. Knockdown or overexpression of MARCH5 in HCC cells was determined by in vitro cell proliferation, migration and invasion assays, and in vivo tumor growth and metastasis assays. In addition, the intrinsic mechanisms by which MARCH5 regulates HCC cell growth and metastasis were explored. Results MARCH5 was significantly overexpressed in HCC cells and was closely associated with patients' poor postoperative prognosis. In vivo and in vitro experiments revealed that MARCH5 significantly promoted the increase and invasive and migratory ability of hepatocellular carcinoma cells, which was mainly due to the promotion of autophagy by MARCH5. Mechanistic studies revealed that MARCH5 promoted autophagy through ubiquitination degradation of p53 leading to malignant progression of hepatocellular carcinoma. Conclusion Our findings suggest that MARCH5 plays a critical oncogenic role in HCC cells, which provides experimental evidence for the use of MARCH5 as a potential target for HCC therapy.

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Section: Discussionmentioning

confidence: 95%

MARCH5 promotes hepatocellular carcinoma progression by inducing p53 ubiquitination degradation

Cai,

Gao,

Yan

et al. 2024

J Cancer Res Clin Oncol

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“…We collected TNF+ Tregs and TNF- Tregs sorted from tumor tissues and GM tissues by flow cytometry sorting. IL13 is involved in the maintenance of cellular stemness, and our previous study demonstrated that IL13 promotes tumor stemness ( 21 ). In addition, high IL-13 levels were closely associated with a high level of Tregs in the tumor microenvironment ( 22 ).…”

Section: Resultsmentioning

confidence: 99%

“…IL13 contributes to the oncogenic effects of renal cell carcinoma and chronic lymphocytic leukemia ( 32 ). In addition, IL-13 promotes the biosynthesis of cytidine deaminase in colonic epithelial cells, conferring the potential to activate the inflammatory-cancer transition in the intestine ( 21 ). Until now, there has been no evidence suggesting that IL-13 can directly enhance the stemness of gastric cancer cells.…”

Section: Discussionmentioning

confidence: 99%

TNF+ regulatory T cells regulate the stemness of gastric cancer cells through the IL13/STAT3 pathway

et al. 2023

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Regulatory T cells (Tregs) are an important component of the tumor microenvironment; however, the interaction between Tregs and gastric cancer cells is not completely understood. Recent studies have shown that Tregs participate in cancer cell stemness maintenance. In this study, we performed single-cell RNA sequencing of gastric cancer and adjacent tissues and found that Tregs with high TNF expression were recruited to gastric cancer tissues and were significantly correlated with patient survival. TNF+ Tregs significantly contribute to tumor growth and progression. Our studies have further demonstrated that TNF+ Tregs promote the stemness of gastric cancer cells through the IL13/STAT3 pathway. Therefore, blocking the interaction between TNF+ Tregs and gastric cancer cells may be a new approach in the treatment of gastric cancer.

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“…Recently, IL13RA2 expression has been examined in plentiful cancers. IL-13/IL-13RA2 aggravates tumorigenesis of colorectal cancer stem cells through accelerating p53 ubiquitination [8]. IL13RA2 knockdown inhibits the migration of papillary thyroid carcinoma cells by regulating epithelial-mesenchymal transition (EMT) [9].…”

Section: Introductionmentioning

confidence: 99%

IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway

LIU,

MA,

et al. 2024

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Background: Interleukin 13 receptor subunit alpha 2 (IL13RA2) plays an essential role in the progression of many cancers. However, the role of IL13RA2 in infantile haemangioma (IH) is still unknown. Materials and Methods: IL13RA2 expression in IH tissues was analyzed using western blot, qRT-PCR, and immunofluorescence. The role of IL13RA2 in haemangioma-derived endothelial cells (HemECs) was determined following knockdown or overexpression of IL13RA2 using CCK-8, colony formation, apoptosis, wound healing, tubule formation, Transwell, and western blot. Results: IL13RA2 expression was upregulated in IH tissues. IL13RA2 overexpression promoted proliferation, migration, and invasion of HemECs and induced glycolysis, which was confirmed with a glycolysis inhibitor. Specifically, IL13RA2 interacted with β-catenin and activated the Wnt/β-catenin pathway in HemECs, which were involved in the above-mentioned effects of IL13RA2. Conclusions: These findings revealed that targeting IL13RA2 is a potential therapeutic approach for IH.

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IL-13/IL-13RA2 signaling promotes colorectal cancer stem cell tumorigenesis by inducing ubiquitinated degradation of p53

Cited by 14 publications

References 41 publications

MARCH5 promotes hepatocellular carcinoma progression by inducing p53 ubiquitination degradation

MARCH5 promotes hepatocellular carcinoma progression by inducing p53 ubiquitination degradation

TNF+ regulatory T cells regulate the stemness of gastric cancer cells through the IL13/STAT3 pathway

IL13RA2 promotes progression of infantile haemangioma by activating glycolysis and the Wnt/β-catenin signaling pathway

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