The FBXW7–KMT2 axis in cancer-associated fibroblasts controls tumor growth via an epigenetic-paracrine mechanism

L Lu Yin (Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education) of the Second Affiliated Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine) J Jiagui Zhang (Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education) of the Second Affiliated Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine) Z Zhipeng Zhu (Institute of Medical Innovation and Research, Peking University 3rd Hospital) X Xiaojuan Peng (Shanghai Institute of Precision Medicine, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine) H Huiyin Lan (Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education) of the Second Affiliated Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine) A Alex Ayoub (Department of Pathology, University of Michigan) M Mingjia Tan B Bo Zhou Y Yaohui He (Fujian Provincial Key Laboratory of Innovative Drug Target Research, School of Pharmaceutical Sciences, Xiamen University) S Siyuan Wang Y Yan Lu W Wen Liu X Xiufang Xiong J Jing Huang Y Yali Dou (Department of Medicine, University of Southern California) F Fengbiao Mao (Institute of Medical Innovation and Research, Peking University 3rd Hospital) Y Yi Sun

Abstract

F-box and WD repeat domain-containing 7 (FBXW7) is a tumor suppressor that targets various oncoproteins for degradation, but its role in modulating cancer-associated fibroblasts (CAFs) in the tumor microenvironment remains elusive. Here, we report that FBXW7 expression is gradually downregulated in CAFs during the progression of human pancreatic and lung cancers. Mechanically, FBXW7 inhibits histone lysine methyltransferase 2 (KMT2) methyltransferase activity via retinoblastoma binding protein 5 (RbBP5) binding, whereas FBXW7 depletion abrogates the binding to activate KMT2, leading to increased H3K4 methylations and global upregulation of gene expression. Activation of the interleukin-17 (IL-17) signaling pathway triggers the secretion of cytokines and chemokines to promote migration, invasion, and sphere formation of lung cancer cells. Coinjection of Fbxw7-depleted mouse embryonic fibroblasts with cancer cells enhances in vivo tumor growth, demonstrating a paracrine effect. Hypoxia downregulates CAF FBXW7 via ETS proto-oncogene 1 (ETS1) to increase H3K4 methylation, whereas conditioned media from hypoxia-exposed CAFs promotes migration and invasion of pancreatic cancer cells, highlighting FBXW7’s tumor-suppressing role through KMT2 inactivation.

Article Details

Volume / Issue Vol. 122, Issue 13
Published April 01, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (17)

L

Lu Yin

Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education) of the Second Affiliated Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine

J

Jiagui Zhang

Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education) of the Second Affiliated Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine

Z

Zhipeng Zhu

Institute of Medical Innovation and Research, Peking University 3rd Hospital

X

Xiaojuan Peng

Shanghai Institute of Precision Medicine, Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine

H

Huiyin Lan

Cancer Institute (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education) of the Second Affiliated Hospital and Institute of Translational Medicine, Zhejiang University School of Medicine

A

Alex Ayoub

Department of Pathology, University of Michigan

M

Mingjia Tan

B

Bo Zhou

Y

Yaohui He

Fujian Provincial Key Laboratory of Innovative Drug Target Research, School of Pharmaceutical Sciences, Xiamen University

S

Siyuan Wang

Y

Yan Lu

W

Wen Liu

X

Xiufang Xiong

J

Jing Huang

Y

Yali Dou

Department of Medicine, University of Southern California

F

Fengbiao Mao

Institute of Medical Innovation and Research, Peking University 3rd Hospital

Y

Yi Sun