乳腺癌
氧化脂质
癌症研究
乳腺肿瘤
脂肪细胞
内分泌学
内科学
癌症
信号转导
生物
脂肪组织
分泌物
脂质代谢
医学
类有机物
脂质信号
肥胖
机制(生物学)
乳腺
癌细胞
细胞生物学
细胞生长
作者
Meghan C. Curtin,Abigail E. Jackson,Mark D. Lee,Elisabeth A. Brown,J. Alan Maschek,David Henry Lum,James Eric Cox,Alana L. Welm,Keren I. Hilgendorf
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2026-09-10
卷期号:393 (6816): eaea4287-eaea4287
被引量:2
标识
DOI:10.1126/science.aea4287
摘要
Obesity increases breast cancer risk and tumor aggressiveness, yet the mechanisms underlying this association remain unclear. In this work, we identify a tumor-suppressive lipid signaling pathway in which mammary adipocytes secrete the oxylipin 9S-hydroxyoctadecadienoic acid (9S-HODE). 9S-HODE induces ferroptosis in breast cancer cells by disrupting iron homeostasis. Adipocytes in obese mammary tissue produce less 9S-HODE, and tumors in obese mice exhibit reduced ferroptosis. Accordingly, ferroptosis inhibition accelerates tumor growth in lean mice, and restoring 9S-HODE suppresses tumor growth in obese mice. In humans, mammary 9S-HODE content is inversely correlated with body mass index, and 9S-HODE inhibits patient-derived breast cancer organoid growth. These findings identify the loss of adipocyte-derived 9S-HODE as a mechanism by which obesity promotes breast cancer and suggest that the restoration of ferroptosis-inducing lipid signaling may be a therapeutic strategy.
科研通智能强力驱动
Strongly Powered by AbleSci AI