SWI/SNF ATPase silenced HLF potentiates lung metastasis in solid cancers

J Jin Zhou (Department of Oncology Sichuan Cancer Hospital Chengdu China) A Austin Hepperla J Jeremy M. Simon K Kangsan Kim Q Qing Hu (State Key Laboratory of Green Chemical Engineering and Industrial Catalysis, Joint International Research Laboratory of Precision Chemistry and Molecular Engineering, Feringa Nobel Prize Scientist Joint Research Center, School of Chemistry and Molecular Engineering) C Chuanhai Zhang L Lei Dong (Quantitative Biomedical Research Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.) L Lianxin Hu C Cheng Zhang C Chengheng Liao A Alice Fang Y Yayoi Adachi H Haoyong Fu T Tao Wang Q Qian Liang F Fangzhou Zhao (Department of Chemistry, McGill University, 801 Sherbrooke Street. W, Montreal, Quebec H3A0B8, Canada) H Hongyi Liu M Masashi Takeda J Jun Fang H Hua Zhong (Department of Chemistry, National University of Singapore, 3 Science Drive 3, Singapore 117543, Republic of Singapore) P Peter Ly L Lu Wang P Payal Kapur L Lin Xu (Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.) L Liwei Jia S Srinivas Malladi J James Brugarolas M M. Celeste Simon B Bo Li Q Qing Zhang

Abstract

Abstract Metastasis is the main cause of cancer-related deaths, yet the underlying mechanisms remain elusive. Here, using clear cell renal cell carcinoma (ccRCC), a tumor type with frequent lung metastases, we conduct an in vivo genome-wide CRISPR-Cas9 screen and identify HLF as a potent suppressor of lung metastasis. HLF depletion enhances ccRCC cell migration and lung metastasis, whereas HLF overexpression abrogates these effects. In ccRCC patients, HLF expression is reduced at metastatic sites and associates with epigenetic silencing mediated by the SWI/SNF ATPase subunit BRG1. HLF levels negatively correlate with migration potential in collagen. Mechanistically, HLF regulates LPXN expression, modulating the integration of collagen’s mechanical cues with the actin cytoskeleton through Paxillin, thereby suppressing cancer cell migration and lung metastasis. Overexpression of HLF or pharmacological inhibition of BRG1 reduces cell invasion across multiple cancer types. Our findings suggest that targeting the BRG1-HLF axis offers a promising therapeutic strategy for combating metastatic cancers.

Article Details

Volume / Issue Vol. 16, Issue 1
Published June 05, 2025
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (30)

J

Jin Zhou

Department of Oncology Sichuan Cancer Hospital Chengdu China

A

Austin Hepperla

J

Jeremy M. Simon

K

Kangsan Kim

Q

Qing Hu

State Key Laboratory of Green Chemical Engineering and Industrial Catalysis, Joint International Research Laboratory of Precision Chemistry and Molecular Engineering, Feringa Nobel Prize Scientist Joint Research Center, School of Chemistry and Molecular Engineering

C

Chuanhai Zhang

L

Lei Dong

Quantitative Biomedical Research Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.

L

Lianxin Hu

C

Cheng Zhang

C

Chengheng Liao

A

Alice Fang

Y

Yayoi Adachi

H

Haoyong Fu

T

Tao Wang

Q

Qian Liang

F

Fangzhou Zhao

Department of Chemistry, McGill University, 801 Sherbrooke Street. W, Montreal, Quebec H3A0B8, Canada

H

Hongyi Liu

M

Masashi Takeda

J

Jun Fang

H

Hua Zhong

Department of Chemistry, National University of Singapore, 3 Science Drive 3, Singapore 117543, Republic of Singapore

P

Peter Ly

L

Lu Wang

P

Payal Kapur

L

Lin Xu

Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.

L

Liwei Jia

S

Srinivas Malladi

J

James Brugarolas

M

M. Celeste Simon

B

Bo Li

Q

Qing Zhang