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Minggang Fang PhD

TitleAssistant Professor
InstitutionUniversity of Massachusetts Medical School
DepartmentMolecular, Cell and Cancer Biology
AddressUniversity of Massachusetts Medical School
364 Plantation Street, Room 670B
Worcester MA 01605
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    Other Positions
    InstitutionUMMS - School of Medicine
    DepartmentMolecular, Cell and Cancer Biology


    Collapse Biography 
    Collapse education and training
    Huazhong Agricultural University, Wuhan, , ChinaBSAgriculture
    Wuhan University, Wuhan, , ChinaMSScience
    University of British Columbia, Vancouver, BC, CanadaPHDPhilosophy

    Collapse Overview 
    Collapse overview

    My research at UMass Medical School is directed toward to understanding the molecular basis of dysregulation of transcription and gene silencing in disease models using the cutting edge tools. I have extensively used transcription-based approaches and functional screens to identify new genes and regulatory pathways involved in neurological diseases and cancers.


    1. Epigenetic silencing in cancer. I have used transcription-based approaches and functional screens to identify new genes and transcriptional regulatory pathways involved in cancer. More recently, I have made significant contributions to our understanding of oncogene-directed epigenetic silencing. To our knowledge, we are the only group that has used large-scale RNAi screening to identify factors involved in epigenetic silencing (Serra et al., 2014; Fang et al., 2014; Fang et al, 2016) and then, through RNAi-based epistasis experiments, order them into pathways. Accordingly, our work has singularly delineated highly specific pathways that are initiated by oncoproteins and culminate in transcriptional silencing of tumor suppressor genes to promote transformation. Furthermore, the pathways we have identified are directly linked to cellular transformation, have enhanced our understanding of how normal cells become cancerous, and have revealed new therapeutic targets.


    2. Drug targets of Fragile X syndrome and Friedreich's Ataxia. Fragile X Syndrome (FXS) is the most common genetic form of mental retardation, and occurs in approximately 1 in 4,000 males and 1 in 8,000 females. To date, no specific and effective therapy exists for FXS, and current treatments are only directed to improve behavioral symptoms. Thus, there is a general need for the development of novel compositions and methods for treating FXS. Through candidate-based RNAi screen and compound screens, , I have identified 7 new drug targets and 6 novel small molecules to rescue FXS (US patent). Friedreich’s Ataxia (FRDA) is a lethal autosomal recessive neurodegenerative disorder caused by the homozygous GAA repeat expansion in the first intron of frataxin gene. FRDA is the most common genetic form of ataxia, and occurs in approximately 1 in 50,000 people. Symptoms typically first appear at 5-15 years of age, followed by progressive neurodegeneration. Typically, within 10 years following the onset of symptoms, the patient is wheelchair bound. The disease affects multiple organs, including the heart and pancreas. Patients have a shortened life expectancy, with most patients dying of cardiac failure. To date, there is no effective therapy for FRDA. Taking similar approaches to FXS, I have identified 10 epigenetic factors as drug targets and 23 novel compounds to rescue the functional defect of FRDA neurons (US patent).


    3. Mechanisms on Genomic Instability. Genomic instability is a hallmark of cancer. My recent study has shown that MEN1 is a melanoma tumor suppressor whose loss elevates mutation rate (Fang et al, 2013). To screen the genes whose loss increases the mutation rates, I have recently performed a genome-wide loss of function RNAi screen and identified 72 factors whose knockdown increase the mutation rate. These proteins are tumor suppressors, transcription factors, regulate apoptosis, autophagy and cell cycle, or play roles in cellular signal transduction, chromosomal segregation, or are functionally unknown. My further studies demonstrate one candidate CRTC2 is a lymphoma tumor suppressor gene and promotes genomic integrity by stimulating transcription of mismatch repair genes (Fang et al, 2015). My follow-up studies on another candidate TDP43 reveal Amyotrophical Lateral Sclerosis with TDP43 loss of function is deficient to homology-directed DNA repair by down-regulating homologous recombination genes (Fang et al, in prep).




    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
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    1. Fang M, Hutchinson L, Deng A, Green MR. Common BRAF(V600E)-directed pathway mediates widespread epigenetic silencing in colorectal cancer and melanoma. Proc Natl Acad Sci U S A. 2016 Feb 2; 113(5):1250-5. PMID: 26787892.
      View in: PubMed
    2. Fang M, Pak ML, Chamberlain L, Xing W, Yu H, Green MR. The CREB Coactivator CRTC2 Is a Lymphoma Tumor Suppressor that Preserves Genome Integrity through Transcription of DNA Mismatch Repair Genes. Cell Rep. 2015 Jun 9; 11(9):1350-7. PMID: 26004186.
      View in: PubMed
    3. Fang M, Ou J, Hutchinson L, Green MR. The BRAF oncoprotein functions through the transcriptional repressor MAFG to mediate the CpG Island Methylator phenotype. Mol Cell. 2014 Sep 18; 55(6):904-15. PMID: 25219500.
      View in: PubMed
    4. Serra RW, Fang M, Park SM, Hutchinson L, Green MR. A KRAS-directed transcriptional silencing pathway that mediates the CpG island methylator phenotype. Elife. 2014 Mar 12; 3:e02313. PMID: 24623306.
      View in: PubMed
    5. Fang M, Xia F, Mahalingam M, Virbasius CM, Wajapeyee N, Green MR. MEN1 is a melanoma tumor suppressor that preserves genomic integrity by stimulating transcription of genes that promote homologous recombination-directed DNA repair. Mol Cell Biol. 2013 Jul; 33(13):2635-47. PMID: 23648481.
      View in: PubMed
    6. Maston GA, Zhu LJ, Chamberlain L, Lin L, Fang M, Green MR. Non-canonical TAF complexes regulate active promoters in human embryonic stem cells. Elife. 2012 Nov 13; 1:e00068. PMID: 23150797.
      View in: PubMed
    7. Peng K, van Lent JW, Boeren S, Fang M, Theilmann DA, Erlandson MA, Vlak JM, van Oers MM. Characterization of novel components of the baculovirus per os infectivity factor complex. J Virol. 2012 May; 86(9):4981-8. PMID: 22379094.
      View in: PubMed
    8. Nie Y, Fang M, Erlandson MA, Theilmann DA. Analysis of the autographa californica multiple nucleopolyhedrovirus overlapping gene pair lef3 and ac68 reveals that AC68 is a per os infectivity factor and that LEF3 is critical, but not essential, for virus replication. J Virol. 2012 Apr; 86(7):3985-94. PMID: 22278232.
      View in: PubMed
    9. Nie Y, Fang M, Theilmann DA. Autographa californica multiple nucleopolyhedrovirus core gene ac92 (p33) is required for efficient budded virus production. Virology. 2011 Jan 5; 409(1):38-45. PMID: 20965540.
      View in: PubMed
    10. Fang M, Nie Y, Harris S, Erlandson MA, Theilmann DA. Autographa californica multiple nucleopolyhedrovirus core gene ac96 encodes a per Os infectivity factor (PIF-4). J Virol. 2009 Dec; 83(23):12569-78. PMID: 19759145.
      View in: PubMed
    11. Fang M, Nie Y, Theilmann DA. Deletion of the AcMNPV core gene ac109 results in budded virions that are non-infectious. Virology. 2009 Jun 20; 389(1-2):66-74. PMID: 19411088.
      View in: PubMed
    12. Fang M, Nie Y, Theilmann DA. AcMNPV EXON0 (AC141) which is required for the efficient egress of budded virus nucleocapsids interacts with beta-tubulin. Virology. 2009 Mar 15; 385(2):496-504. PMID: 19155039.
      View in: PubMed
    13. Nie Y, Fang M, Theilmann DA. AcMNPV AC16 (DA26, BV/ODV-E26) regulates the levels of IE0 and IE1 and binds to both proteins via a domain located within the acidic transcriptional activation domain. Virology. 2009 Mar 15; 385(2):484-95. PMID: 19150105.
      View in: PubMed
    14. Fang M, Nie Y, Dai X, Theilmann DA. Identification of AcMNPV EXON0 (ac141) domains required for efficient production of budded virus, dimerization and association with BV/ODV-C42 and FP25. Virology. 2008 May 25; 375(1):265-76. PMID: 18313716.
      View in: PubMed
    15. Fang M, Dai X, Theilmann DA. Autographa californica multiple nucleopolyhedrovirus EXON0 (ORF141) is required for efficient egress of nucleocapsids from the nucleus. J Virol. 2007 Sep; 81(18):9859-69. PMID: 17626083.
      View in: PubMed
    16. Deng F, Wang R, Fang M, Jiang Y, Xu X, Wang H, Chen X, Arif BM, Guo L, Wang H, Hu Z. Proteomics analysis of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus identified two new occlusion-derived virus-associated proteins, HA44 and HA100. J Virol. 2007 Sep; 81(17):9377-85. PMID: 17581982.
      View in: PubMed
    17. Fang M, Nie Y, Wang Q, Deng F, Wang R, Wang H, Wang H, Vlak JM, Chen X, Hu Z. Open reading frame 132 of Helicoverpa armigera nucleopolyhedrovirus encodes a functional per os infectivity factor (PIF-2). J Gen Virol. 2006 Sep; 87(Pt 9):2563-9. PMID: 16894194.
      View in: PubMed
    18. Nie Y, Wang Q, Liang C, Fang M, Yu Z, Chen X. Characterization of ORF2 and its encoded protein of the Helicoverpa armigera nucleopolyhedrovirus. Virus Res. 2006 Mar; 116(1-2):129-35. PMID: 16249044.
      View in: PubMed
    19. Fang M, Wang H, Wang H, Yuan L, Chen X, Vlak JM, Hu Z. Open reading frame 94 of Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus encodes a novel conserved occlusion-derived virion protein, ODV-EC43. J Gen Virol. 2003 Nov; 84(Pt 11):3021-7. PMID: 14573807.
      View in: PubMed
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