39181-Bellail, Anita
Faculty

Anita Bellail

Assistant Professor of Pathology & Laboratory Medicine

Bio

Dr. Bellail grew up along the coast of Normandy in France. She received her BA in Cell Biology, MSc in Biochemistry and PhD in neuroscience from the University of Caen in France. Under the support of the French Association for Cancer Research scholarship,, she came to the US in 2002 and started her postdoctoral training at the Winship Cancer Institute of Emory University, Atlanta.

Dr. Bellail became Assistant Professor of Neurology and Neurological Surgery of the Montreal Neurological Institute at McGill University in Canada in 2013. She moved back to the US and worked at the Henry Ford Health System Research Institute, Michigan.  In January 2018, Dr. Bellail was recruited to the Indiana University School of Medicine as an Assistant Professor of Pathology and Laboratory Medicine.

Dr. Bellail started her research on ubiquitin posttranslational modification pathways in regulation of cancer cell programed death in human cancer. Her laboratory then demonstrated that the posttranslational pathway of small ubiquitin modifier-1 (SUMO1) drives the cell cycle and cancer progression. In a cancer cell-based drug screening of NCI small molecule laboratory, her team identified the SUMO1 inhibition compound (SMIC1). Her current research aims to develop SMIC1 as a new anticancer drug for clinical cancer therapy and unveil SMIC1 targeted molecular pathways in human cancer.

Key Publications

http://www.ncbi.nlm.nih.gov/myncbi/browse/collection/47731534/?sort=date&direction=ascending

Titles & Appointments

  • Assistant Professor of Pathology & Laboratory Medicine
  • Research

    My research is centered on the posttranslational modifications of ubiquitin (UB) and small ubiquitin-like modifier (SUMO) for development of UB and SUMO targeted new anticancer drugs. Initially, I investigated the role of the UB E3 ligase A20 in cancer resistance to the treatment of tumor necrosis factor-related apoptosis ligand (TRAIL). Then, we demonstrated that SUMO1 modification pathway drives the cell cycle and cancer progression. In cancer cell-based drug screening of NCI compounds library, we identified the small molecule SUMO1 inhibition compound (SMIC1) and demonstrated its therapeutic potential in treatment of patient derived cancer xenografts (PDXs). CRISPR/CAS9 genome wide screening revealed the ubiquitination pathway that SMIC1 activates for SUMO1 protein degradation.

     

    My current research effort is focused on the following three projects. The 1st project aim to delineate the ubiquitination pathway for SUMO1 degradation and establish the novel concept that UB-SUMO cross-talk controls cancer growth. The 2nd project is to improve the potency and drug-like features of the hit compound SMIC1 through medical chemistry for its clinical development as a new anticancer drug. The 3rd project is to develop TRAIL and SMIC1 combined treatment of cancers. My lab has recently found that the death receptor-5 (DR5) of TRAIL is modified by SUMO1 and DR5-SUMO1 conjugation results in cancer resistance to TRAIL treatment. SMIC1 treatment abolishes DR5-SUMO1 conjugation and leads to TRAIL-induced apoptosis. This study will prove the new cancer therapy in the combination of TRAIL and SMIC1.

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