Honors & Awards


  • Research journey interview featured by the journal Development, Development (2020)
  • Senior Research Fellow Award, Department of Biotechnology, India (2019-2020)
  • Best Oral Presentation Award, UNESCO-Regional Centre for Biotechnology Open day, Faridabad, India (2018)
  • Travel Award, Tsakura Science Club, Tsakura, Japan (2017)
  • Senior Research Fellow Award, Indian Council of Medical Research, India (2014-2019)
  • Junior Research Fellow Award, Indian Council of Agriculture Research, India (2013-2014)
  • National Eligibility Test Award, University Grant Commission, India (2013)
  • Best Poster Presentation Award, National Symposium on Emerging Trends in Biotechnology Research (2013)
  • Institutional fellowship, Indian Veterinary Research Institute, Izzatnagar, India (2011-2013)

Professional Education


  • Master of Science, Indian Veterinary Research Institute (2013)
  • Doctor of Philosophy, Manipal Academy of Higher Education (2020)
  • Doctor of Veterinary Medicine, G B Pant University Of Agriculture (2011)
  • PhD, UNESCO-Regional Centre for Biotechnology, Faridabad, India, Developmental Genetics (2020)
  • MVSc, Indian Veterinary Research Institute, Izzatnagar, India, Animal Biotechnology (2013)
  • BVSc & AH, Govind Ballabh Pant University of Agriculture and Technology, India, Veterinary Science (2011)

Stanford Advisors


All Publications


  • The Wnt-pathway corepressor TLE3 interacts with the histone methyltransferase KMT1A to inhibit differentiation in Rhabdomyosarcoma. Oncogene Kalita, B., Sahu, S., Bharadwaj, A., Panneerselvam, L., Martinez-Cebrian, G., Agarwal, M., Mathew, S. J. 2024

    Abstract

    Rhabdomyosarcoma tumor cells resemble differentiating skeletal muscle cells, which unlike normal muscle cells, fail to undergo terminal differentiation, underlying their proliferative and metastatic properties. We identify the corepressor TLE3 as a key regulator of rhabdomyosarcoma tumorigenesis by inhibiting the Wnt-pathway. Loss of TLE3 function leads to Wnt-pathway activation, reduced proliferation, decreased migration, and enhanced differentiation in rhabdomyosarcoma cells. Muscle-specific TLE3-knockout results in enhanced expression of terminal myogenic differentiation markers during normal mouse development. TLE3-knockout rhabdomyosarcoma cell xenografts result in significantly smaller tumors characterized by reduced proliferation, increased apoptosis and enhanced differentiation. We demonstrate that TLE3 interacts with and recruits the histone methyltransferase KMT1A, leading to repression of target gene activation and inhibition of differentiation in rhabdomyosarcoma. A combination drug therapy regime to promote Wnt-pathway activation by the small molecule BIO and inhibit KMT1A by the drug chaetocin led to significantly reduced tumor volume, decreased proliferation, increased expression of differentiation markers and increased survival in rhabdomyosarcoma tumor-bearing mice. Thus, TLE3, the Wnt-pathway and KMT1A are excellent drug targets which can be exploited for treating rhabdomyosarcoma tumors.

    View details for DOI 10.1038/s41388-023-02911-3

    View details for PubMedID 38177411

    View details for PubMedCentralID 4462130

  • TLE4 regulates muscle stem cell quiescence and skeletal muscle differentiation JOURNAL OF CELL SCIENCE Agarwal, M., Bharadwaj, A., Mathew, S. J. 2022; 135 (4)

    Abstract

    Muscle stem (satellite) cells express Pax7, a key transcription factor essential for satellite cell maintenance and adult muscle regeneration. We identify the corepressor transducin-like enhancer of split-4 (TLE4) as a Pax7 interaction partner expressed in quiescent satellite cells under homeostasis. A subset of satellite cells transiently downregulate TLE4 during early time points following muscle injury. We identify these to be activated satellite cells, and that TLE4 downregulation is required for Myf5 activation and myogenic commitment. Our results indicate that TLE4 represses Pax7-mediated Myf5 transcriptional activation by occupying the -111 kb Myf5 enhancer to maintain quiescence. Loss of TLE4 function causes Myf5 upregulation, an increase in satellite cell numbers and altered differentiation dynamics during regeneration. Thus, we have uncovered a novel mechanism to maintain satellite cell quiescence and regulate muscle differentiation mediated by the corepressor TLE4.

    View details for DOI 10.1242/jcs.256008

    View details for Web of Science ID 000762675900001

    View details for PubMedID 35099008