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Search Results to Minggang Fang PhD

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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).

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  • Oncogenes