ArticleInternational journal of biological sciences2026
Cancer-associated adipocytes confer CDK4/6 inhibitor resistance in ER+ breast cancer through an IL-6/STAT3/SREBF2 axis coupled with cholesterol metabolism and cell cycle reprogramming.
Article in International journal of biological sciences, 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
Cancer-associated adipocytes (CAAs) within the tumor microenvironment (TME) critically regulate oncogenic progression. However, the mechanistic basis underlying CAAs-mediated CDK4/6 inhibitor (CDK4/6i) resistance in estrogen receptor-positive (ER+) breast cancer remains elusive. In this study, we revealed that CAAs supernatant demonstrated enhanced capacity to induce CDK4/6i resistance in ER+ breast cancer cells compared to NAs-derived conditioned medium. Through integrated RNA sequencing and cytokine microarray screening, we identified marked upregulation of IL-6 in both CAAs and their conditioned media. Mechanistically, CAAs-derived IL-6 activates the JAK-STAT3 axis, leading to transcriptional upregulation of SREBF2, which directly drives CDK4/6i resistance through HMGCR-mediated lipid metabolism and CDKN2C-mediated cell cycle progression (IL-6
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