ArticleWorld journal of gastrointestinal oncology2025
Interleukin-22 promotes cancer stemness and chemotherapy resistance in colorectal cancer
Article in World journal of gastrointestinal oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Oncogenic Role of Prostate Stem Cell Antigen (PSCA) in Colorectal Cancer: Implications for Targeted Therapy.Current issues in molecular biology · 2026Article
- Exploratory Study of Serum IL-22 and CD163+ Macrophages in Glioblastoma Multiforme.Medicina (Kaunas, Lithuania) · 2026Article
- Fibroblasts selectively modulate immune cell-derived cytokine effects on tumor cells in colorectal cancer.Frontiers in immunology · 2026Article
- Plasticity and antigen presentation by group 3 innate lymphoid cells in colorectal cancer.Frontiers in immunology · 2026Review
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Authors and funding
4 authors.
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Abstract
backgroundInterleukin-22 (IL-22) belongs to the IL-10 cytokine family, recognized for its ability to modulate diverse immune responses. Previous studies have indicated that IL-22 promotes cancer advancement and metastasis. However, the precise function of IL-22 in colorectal cancer (CRC) remains unclear.
aimTo investigate the role of IL-22 in promoting stem cell-like characteristics and chemotherapy resistance in CRC cells, as well as to elucidate the mechanisms underlying these effects.
methodsHCT116 cells were treated with IL-22 (50 ng/mL) and oxaliplatin (L-OHP, 5 μg/mL). A series of functional assays - including cell counting kit-8 assay, tumor sphere formation assay, and cell apoptosis assay - were conducted to assess the effects of IL-22 on cell viability and stem cell-like characteristics. The expression of stemness-related markers (SOX2, Oct4, NANOG, and Bmi-1) was examined using Western blot analysis. Additionally, the total and phosphorylated levels of epidermal growth factor receptor (EGFR), protein kinase B (AKT), and extracellular signal-regulated kinase (ERK) were evaluated by Western blot. An EGFR inhibitor, osimertinib (Osi), was used to assess the pathway's functional relevance.
resultsIL-22 treatment promotes CRC cell proliferation, enhances sphere formation, and elevates the expression of stem cell markers, including SOX2, Oct4, NANOG, and Bmi-1. IL-22 treatment increases the phosphorylation of EGFR, AKT, and ERK. Additionally, IL-22 treatment mitigates the cytotoxic effects and the ability to induce apoptosis of L-OHP. Furthermore, IL-22 treatment activated the EGFR/ERK signaling pathway by increasing the phosphorylation of EGFR, AKT, and ERK. Importantly, the use of the EGFR inhibitor Osi significantly counteracted the chemoresistance induced by IL-22 in CRC cells.
conclusionIL-22 promotes tumor growth and induces chemotherapy resistance in CRC cells by activating the EGFR/ERK signaling pathway. These findings suggest that targeting IL-22 or its downstream signaling may offer novel therapeutic strategies in CRC.
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