Reactivation of PTEN tumor suppressor for cancer treatment through inhibition of a MYC-WWP1 inhibitory pathway-Reference-Cited by-同舟云学术

Reactivation of PTEN tumor suppressor for cancer treatment through inhibition of a MYC-WWP1 inhibitory pathway

Published:2019-05-17 Issue:6441 Volume:364 Page:
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Lee Yu-Ru¹²^ORCID,Chen Ming¹²^ORCID,Lee Jonathan D.¹²,Zhang Jinfang³,Lin Shu-Yu⁴,Fu Tian-Min⁵⁶^ORCID,Chen Hao⁷⁸^ORCID,Ishikawa Tomoki¹²,Chiang Shang-Yin⁴⁹,Katon Jesse¹²^ORCID,Zhang Yang¹²,Shulga Yulia V.¹²^ORCID,Bester Assaf C.¹²,Fung Jacqueline¹²,Monteleone Emanuele¹²¹⁰^ORCID,Wan Lixin³¹¹^ORCID,Shen Chen⁵⁶,Hsu Chih-Hung⁷⁸¹²^ORCID,Papa Antonella¹³^ORCID,Clohessy John G.¹²¹⁴^ORCID,Teruya-Feldstein Julie¹⁵,Jain Suresh¹⁶,Wu Hao⁵⁶^ORCID,Matesic Lydia¹⁷^ORCID,Chen Ruey-Hwa⁴⁹,Wei Wenyi³^ORCID,Pandolfi Pier Paolo¹²^ORCID

Affiliation:

1. Cancer Research Institute, Beth Israel Deaconess Cancer Center, Harvard Medical School, Boston, MA 02215, USA.

2. Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

3. Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

4. Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan.

5. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.

6. Program in Cellular and Molecular Medicine, Boston Children’s Hospital, Boston, MA 02115.

7. Division of Newborn Medicine, Boston Children’s Hospital, Boston, MA 02115, USA.

8. Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

9. Institute of Biochemical Sciences, College of Life Science, National Taiwan University, Taipei 106, Taiwan.

10. Department of Molecular Biotechnology and Health Sciences, and GenoBiToUS, Genomics and Bioinformatics Service, University of Turin, Turin, Italy.

11. Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.

12. Department of Public Health, Women’s Hospital, Zhejiang University School of Medicine, Hangzhou 310058, Zhejiang, China.

13. Cancer Program, Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria 3800, Australia.

14. Preclinical Murine Pharmacogenetics Facility and Mouse Hospital, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.

15. Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.

16. Intonation Research Laboratories, Hyderabad, India.

17. Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USA.

Abstract

Supporting tumor suppression The protein PTEN is a phosphatase and tumor suppressor whose activity is often decreased in human cancers. Thus, reactivating such a protein could potentially be an effective therapy against cancer. Lee et al. identified a ubiquitin E3 ligase (WWP1) as a PTEN-interacting protein that modifies PTEN and inhibits its tumor suppressive activity (see the Perspective by Parsons). Depletion of WWP1 increased dimerization and membrane recruitment of PTEN. A natural compound found to be a pharmacological inhibitor of WWP1 inhibited tumor growth in a mouse model of prostate cancer. Thus, reactivation of the tumor suppressor PTEN may provide a strategy for battling tumors. Science , this issue p. eaau0159 ; see also p. 633

Funder

U.S. Department of Defense

NIH Office of the Director

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference53 articles.

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4. Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis

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