ArticleMolecular and cellular biochemistry2026
Context-dependent promotion of epithelial-mesenchymal transition by IL-13Rα2/STAT6 signaling in colorectal cancer.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The precise mechanistic role of Interleukin-13 receptor alpha-2 (IL-13Rα2) in colorectal cancer (CRC) remains elusive, specifically regarding whether it functions as an active signaling receptor or a passive decoy. Its unique role in metastatic phenotypic plasticity remains poorly understood. We identified IL-13Rα2 as a powerful oncogenic signaling hub that significantly increases CRC cell proliferation, migration, and colony formation using shRNA knockdown and CRISPR activation to modify IL-13Rα2 across a range of CRC cell lines with different baseline characteristics. Most importantly, we found that its regulation of the epithelial-mesenchymal transition (EMT) is highly context-dependent. IL-13Rα2 controls the mesenchymal phenotype in highly plastic cells in a partial-EMT (p-EMT) stage (such as SW-480 and SW-620). Its removal completely reverses EMT and collapses core plasticity-driving nodes, such as AGR2 and p63. On the other hand, IL-13Rα2 precisely functions as a phenotypic amplifier limited by the cellular epigenetic landscape in strictly epithelial cells (such as HT-29), where it controls cellular survival but does not initiate EMT. The STAT6 signaling cascade is monopolized by IL-13Rα2. Targeted downregulation eliminates IL-13-induced STAT6 phosphorylation, which in turn causes severe cell cycle dysregulation marked by a delayed G1/S transition and intra-S phase arrest. In conclusion, our research demonstrates that IL-13Rα2 is a crucial, context-dependent signaling receptor that maintains the p-EMT state and malignant progression via the STAT6 axis, making it a precise therapeutic target for advanced, phenotypically plastic colorectal cancer.
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