Nature Communications (Nov 2021)
Opposing transcriptional programs of KLF5 and AR emerge during therapy for advanced prostate cancer
- Meixia Che,
- Aashi Chaturvedi,
- Sarah A. Munro,
- Samuel P. Pitzen,
- Alex Ling,
- Weijie Zhang,
- Josh Mentzer,
- Sheng-Yu Ku,
- Loredana Puca,
- Yanyun Zhu,
- Andries M. Bergman,
- Tesa M. Severson,
- Colleen Forster,
- Yuzhen Liu,
- Jacob Hildebrand,
- Mark Daniel,
- Ting-You Wang,
- Luke A. Selth,
- Theresa Hickey,
- Amina Zoubeidi,
- Martin Gleave,
- Rohan Bareja,
- Andrea Sboner,
- Wayne Tilley,
- Jason S. Carroll,
- Winston Tan,
- Manish Kohli,
- Rendong Yang,
- Andrew C. Hsieh,
- Paari Murugan,
- Wilbert Zwart,
- Himisha Beltran,
- R. Stephanie Huang,
- Scott M. Dehm
Affiliations
- Meixia Che
- Masonic Cancer Center, University of Minnesota
- Aashi Chaturvedi
- Masonic Cancer Center, University of Minnesota
- Sarah A. Munro
- University of Minnesota Supercomputing Institute, University of Minnesota
- Samuel P. Pitzen
- Masonic Cancer Center, University of Minnesota
- Alex Ling
- Department of Experimental and Clinical Pharmacology, University of Minnesota
- Weijie Zhang
- Department of Experimental and Clinical Pharmacology, University of Minnesota
- Josh Mentzer
- Department of Experimental and Clinical Pharmacology, University of Minnesota
- Sheng-Yu Ku
- Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School
- Loredana Puca
- Division of Medical Oncology, Weill Cornell Medicine
- Yanyun Zhu
- Division on Oncogenomics, Oncode Institute, The Netherlands Cancer Institute
- Andries M. Bergman
- Division on Oncogenomics, Oncode Institute, The Netherlands Cancer Institute
- Tesa M. Severson
- Division on Oncogenomics, Oncode Institute, The Netherlands Cancer Institute
- Colleen Forster
- Department of Laboratory Medicine and Pathology, University of Minnesota
- Yuzhen Liu
- Divisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center
- Jacob Hildebrand
- Masonic Cancer Center, University of Minnesota
- Mark Daniel
- Masonic Cancer Center, University of Minnesota
- Ting-You Wang
- The Hormel Institute, University of Minnesota
- Luke A. Selth
- Flinders Health and Medical Research Institute and Flinders Centre for Innovation in Cancer, Flinders University
- Theresa Hickey
- Dame Roma Mitchell Cancer Research Laboratories and Freemasons Foundation Centre for Men’s Health, Adelaide Medical School, The University of Adelaide
- Amina Zoubeidi
- Department of Urologic Sciences, University of British Columbia
- Martin Gleave
- Department of Urologic Sciences, University of British Columbia
- Rohan Bareja
- Englander Institute for Precision Medicine, Weill Cornell Medicine
- Andrea Sboner
- Englander Institute for Precision Medicine, Weill Cornell Medicine
- Wayne Tilley
- Dame Roma Mitchell Cancer Research Laboratories and Freemasons Foundation Centre for Men’s Health, Adelaide Medical School, The University of Adelaide
- Jason S. Carroll
- Cancer Research UK, University of Cambridge
- Winston Tan
- Department of Medicine, Mayo Clinic
- Manish Kohli
- Huntsman Cancer Institute, University of Utah
- Rendong Yang
- Masonic Cancer Center, University of Minnesota
- Andrew C. Hsieh
- Divisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center
- Paari Murugan
- Department of Laboratory Medicine and Pathology, University of Minnesota
- Wilbert Zwart
- Division on Oncogenomics, Oncode Institute, The Netherlands Cancer Institute
- Himisha Beltran
- Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School
- R. Stephanie Huang
- Department of Experimental and Clinical Pharmacology, University of Minnesota
- Scott M. Dehm
- Masonic Cancer Center, University of Minnesota
- DOI
- https://doi.org/10.1038/s41467-021-26612-1
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 15
Abstract
While many treatments for prostate cancer suppress the androgen receptor it becomes reactivated during disease progression. Here, the authors show that a KLF5 transcriptional programme is also activated during treatment and promotes migration and the appearance of a basal cell phenotype.
