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HUA Fang Principal Investigator
Professor

Department :

Department of Pharmacology

Platform :

State Key Laboratory of Bioactive Substance and Function of Natural Medicines;
Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study

Contact Details

Hua Fang's group
huafang@imm.ac.cn
Brief Introduction

Education

08/2000-07/2005: Peking Union Medical College and Chinese Academy of Medical Sciences, Ph.D. in Biochemistry and Molecular Biology

09/1995-07/2000: Shanghai Medical College of Fudan University, B.S. in Clinical Medicine

Professional Experience

12/2017-03/2019: Michigan Medicine, University of Michigan, Department of Surgery

12/2018-present:  Professor, Institute of Materia Medica, CAMS & PUMC

09/2014-11/2018: Associate Professor, Institute of Materia Medica, CAMS & PUMC

08/2005-08/2014: Research Assistant, Institute of Materia Medica, CAMS & PUMC      

Research interests

The adaptability of tumors to the harsh environmental factors, and the intrinsic changes of tumor metabolism are the core theme of tumor research. Hua Fang's current research area is inflammation and metabolic changes in the regulation of tumor intrinsic properties (oncogenic gene expression, stemness etc.) and anti-tumor immune response, as well as the crosstalk between each other. She pays special attention to aberrant protein quality control (UPS and autophagy) in the regulation of these processes.

Achievements

Papers

1. Faciogenital Dysplasia 5 supports cancer stem cell traits in basal-like breast cancer by enhancing EGFR stability.  Sci Transl Med . 13(586):eabb2914, 2021.

2. Loss of optineurin drives cancer immune evasion via palmitoylation-dependent IFNGR1 lysosomal sorting and degradation.  Cancer Discov . doi: 10.1158/2159-8290.CD-20-1571, 2021.

3. TRIB3-EGFR interaction promotes lung cancer progression and defines a therapeutic target.  Nat Commun. , 11(1): 3660, 2020.

4. Disruption of the EGFR-SQSTM1 interaction by a stapled peptide suppresses lung cancer via activating autophagy and inhibiting EGFR signaling.  Cancer Lett . 474:23-35, 2020.

5. TRIB3 Interacts with Beta-catenin and TCF4 to Increase Stem Cell Features of Colorectal Cancer Stem Cells and Tumorigenesis.  Gastroenterology . 156(3):708-721, 2019.

6. Immune Signaling and Autophagy Regulation.  Adv Exp Med Biol . 1206:551-593, 2019.

7. Metformin suppresses melanoma progression by inhibiting KAT5-mediated SMAD3 acetylation, transcriptional activity and TRIB3 expression.  Oncogene . 37(22):2967-2981, 2018

8. Seeking new anti-cancer agents from autophagy-regulating natural products.  J Asian Nat Prod Res. 19(4):305-313, 2017.

9. The regulation of β-catenin activity and function in cancer: therapeutic opportunities. Oncotarget. 8:33972-33989, 2017

10. Diabetes and cancer, common threads and missing links.  Cancer Lett, 374:54-61, 2016.

11. TRB3 links insulin/IGF to tumour promotion by interacting with p62 and impeding autophagic/proteasomal degradation functions.  Nat Commun., 6:7951, 2015.

12. The TRIB3-SQSTM1 interaction mediates metabolic stress-promoted tumorigenesis and progression via suppressing autophagic and proteasomal degradation.  Autophagy , 11:1929-1931, 2015.

13. TRIB3-P62 interaction, diabetes and autophagy.  Oncotarget.  6:34061-34062, 2015.

14. Transport and uptake of clausenamide enantiomers in CYP3A4-transfected Caco-2 cells: An insight into the efflux-metabolism alliance.  Biochem Pharmacol . 98:224-230, 2015.

15. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 2021.  Autophagy . 17(1):1-382, 2021.

16. TRIB3 promotes MYC-associated lymphoma development through suppression of UBE3B-mediated MYC degradation.  Nat Commun.  11(1):6316, 2020.

17. TRIB3 Supports Breast Cancer Stemness by Suppressing FOXO1 Degradation and Enhancing SOX2 Transcription.  Nat Commun.  10:5720, 2019.

18. Targeting Degradation of the Transcription Factor C/EBPβ Reduces Lung Fibrosis by Restoring Activity of the Ubiquitin-Editing Enzyme A20 in Macrophages.  Immunity. 51:522-534, 2019

19. Disrupting the TRIB3-SQSTM1 interaction reduces liver fibrosis by restoring autophagy and suppressing exosome-mediated HSC activation.  Autophagy. 16(5):782-796, 2020

20. Targeting Extracellular Heat Shock Protein 70 Ameliorates Doxorubicin-Induced Heart Failure Through Resolution of Toll-Like Receptor 2-Mediated Myocardial Inflammation.  J Am Heart Assoc. 8:e012338, 2019.

21. Metformin reduces TRIB3 expression and restores autophagy flux: an alternative antitumor action.  Autophagy . 2018;14(7):1278-1279.

22. 1,25-Dihydroxyvitamin D3 protects obese rats from metabolic syndrome via promoting regulatory T cell-mediated resolution of inflammation.  Acta Pharm Sin B.  8:178-187, 2018.

23. TRIB3 Promotes APL Progression through Stabilization of the Oncoprotein PML-RARα and Inhibition of p53-Mediated Senescence.  Cancer Cell . 31:697-710, 2017.

24. BCL6 induces EMT by promoting the ZEB1-mediated transcription repression of E-cadherin in breast cancer cells.  Cancer Lett . 365:190-200, 2015.

Books

1. “Immune Signaling and Autophagy Regulation” Chapter 26 , Autophagy: Biology and Disease , Basic Science. Zheng-Hong Qin Editor. Springer, Science Press Beijing, pp. 551-593, 2019, ISBN 9789811506017.

2. Research Advances in Molecular Mechanisms and Therapeutic Strategies of Metabolic Diseases.  Practical Molecular Pharmacology (2nd Edition), Wang XL (eds.).  Pecking Union Medical College Press, pp 351-382, 2015, ISBN 9787567904118. (Chinese)

3. Flow Cytometry Technique in the Study of Molecular Immunology & Pharmacology. Chen XG (eds.),  The New Techniques and Methods in Pharmacological Research .  Pecking Union Medical College Press, pp 210-240, 2014, ISBN 9787811368758. (Chinese)

4. Use of the tumor Repressor DEDD as a prognostic Marker of Cancer Metastasis. Edited by Martha Robles-Flores (eds.).  Cancer Cell Signaling, Methods and Protocols , 2nd Edition.  Humana Press, pp.197-222, 2014, ISBN 9781493908554.

Honors & Awards

Fang Hua, Winners of 20th CNPHARS-SERVIER Prize.  Chinese Pharmacological Society & Servier, 2016.