Reveals KLF11's role in suppressing lipogenesis and CRC progression, suggesting a new therapeutic avenue.
Colorectal cancer (CRC) remains one of the most frequently diagnosed and lethal malignancies. Recent studies showed that either adipose-derived mesenchymal stem cells (adMSCs) or the extracellular vesicles (EVs) they secrete retarded CRC progression. Here, we investigated the mechanism underlying the role of adMSCs-EVs in CRC. Here, we found that Krüppel-like factor 11 (KLF11) was upregulated in adMSCs-EVs. adMSCs-EVssh-KLF11 (EVs derived from KLF11-depleted adMSCs) effectively promoted lipogenesis, cell viability, proliferation, migration, and invasion of CRC cells, and accelerated tumor growth in mice. Furthermore, KLF11 carried by adMSCs-EVs dampened the PI3K/AKT signaling pathway by transcriptionally repressing sterol o-acyltransferase 1 (SOAT1) expression. SOAT1 knockdown blocked the enhanced lipogenesis, proliferation, migration and invasion induced by adMSCs-EVssh-KLF11. In conclusion, KLF11 derived from adMSCs-EVs inactivated the PI3K/AKT signaling pathway by transcriptionally downregulating SOAT1, therefore suppressing lipogenesis and malignant progression of CRC.
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Yang et al. (2026) studied this question.
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