Mrinal Kanti Ghosh, Ph.D., FNASC, FAScT

Principal Scientist
Cancer Biology & Inflammatory Disorder

Research Interest

Signal Transduction in Cancer & Stem Cells
  • Cancer has a multifaceted character which is inherent in its very origin. Diverse arrays of aberrations are required before a normal cell in your body will defy ‘social behavior’ to fulfill its only purpose – to proliferate – at the expense of you. By then, deep down at the molecular level crucial signalling pathways would have been extensively rewired. Proteins such as p53 and PTEN which keeps scrupulous cellular growth in check are lost functionally; whereas proteins accelerating growth, such as STAT3, β-catenin and c-Myc, are up-regulated. Protein kinases like Akt and CK2 regulate these players by phosphorylation at critical residues that have important bearing upon their functions. Another class of proteins that include E3 ubiquitin ligases like CHIP and deubiquitinases like HAUSP regulate these same players by governing their half-lives. Our lab is interested and actively working on all these aspects of a tumour cell. To understand cancer and to be able to intervene in its progression we concentrate on these most basic mechanisms. An appreciation of these will probably take us one step further in the way to treating cancer.
  • Cross-regulation of Wnt/β-catenin and EGFR Signalling in Cancer: Our aim is to determine the major pathways responsible for the activation and nuclear localization of Stat3 & β-catenin in human cancer & cancer stem cells and study in particular, the involvement of EGFR & Wnt signaling for this regulation. In this context, the mechanism of nuclear accumulation of β-catenin and its subsequent trans-activation of downstream targets also plays a crucial role in cancer development. The unraveling of the potential intersections of these pathways in glioma, breast and prostate cancer may provide novel targets for drug discovery.
  • Role of DEAD Box RNA Helicases in Cancer: RNA Helicases play crucial roles in developmental processes. Recently, it has been implied that its involvement in transcription is very important in cancer progression. In our present study we would like to study the regulation of p68/p72 through EGFR & Wnt signaling and importance in cancer progression.
  • Role of Ubiquitinases and Deubiquitinases in Cancer: Ubiquitin ligases and deubiquitinases play major roles in cellular physiology by modulating half-lives of numerous proteins. Because ubiquitination and deubiquitination events can influence the time a protein spends inside the cell and the space it occupies during that time, a balance between these events is necessary for maintaining cellular homeostasis and normal functioning. Cancer cells are thought to bypass this balance towards a net increase in proliferation and growth. Therefore, understanding these key mechanisms is important for combating cancer.
  • Role of Casein Kinase II in Modulation of Cancer Cell Signaling: Casein Kinase II/CKII is a ubiquitously expressed Ser/Thr kinase present in all cells, with known upregulated activity in Cancers (e.g. Prostate, Brain Breast etc.). Our aim is to study the various oncogenic signalings initiated and modulated by CKII, and decipher the mechanistic detail how such signaling modulation is responsible for oncogenicity of a cell. Presently among various players, we are interested to investigate the crosstalk of CKII with AKT (another well known oncogenic kinase), PML (an important nuclear sequestering protein) and DAXX (an adapter protein).
  • Drug Discovery: Anti-cancer drug discovery from natural products and using target based synthetic peptides.


  • Staff (2003-2005): Dept. of Cancer Biology, Cleveland Clinic Foundation, OHIO, USA.
  • PDF (1997-2003): Dept. of Molecular Biology, Cleveland Clinic Foundation, OHIO, USA. 
  • Ph. D.(2000): University of Calcutta, W.B., India. 

Honours & Awards


Patents & Publications

  1. M Sarkar, V Khare and MK Ghosh* (2016). The DEAD box protein p68: a novel coactivator of Stat3 in mediating oncogenesis. Oncogene (In press). {IF= 7.9}
  2. Sarkar M, Khare V†, Guturi KKN†, Das N and Ghosh MK* (2015). The DEAD box protein p68: a crucial regulator of AKT/FOXO3a signaling axis in oncogenesis. Oncogene 34: 5843–5856. {IF= 8.5}
  3. Das N, Datta N, Chatterjee U and Ghosh MK* (2016). ERα transcriptionally activates CK2α: a pivotal regulator of PML and AKT in oncogenesis. Cell Signal 26: 1725-1734. {IF= 4.3}
  4. Ahmed SF, Das N, Sarkar M, Chatterjee U, Chatterjee S, and Ghosh MK* (2015). Exosome-mediated delivery of the intrinsic C-terminus domain of PTEN protects it from proteasomal degradation and ablates tumorigenesis. Molecular Therapy 23: 255–269. {IF= 6.8} 10.
  5. Bhattacharya S and Ghosh MK* (2015). HAUSP regulates cMyc via deubiquitination of TRRAP. Cell Oncol 38: 265-77. {IF= 3.6}
  6. Ghosh A, et al., (2016). Formulation and antitumorigenic activities of nanoencapsulated nifetepimine: A promising approach in treating triple negative breast carcinoma. Nanomedicine: NBM 12 (2016) 1973–1985. {IF= 6.1}
  7. Guturi KK, Sarkar M, Bhowmik A#,  Das N#  and Ghosh MK* (2015). DEAD box protein p68 is regulated by β-catenin/TCF4 to maintain a positive feedback loop in control of breast cancer progression. Breast Cancer Research 16:496.
  8. Bhattacharya S and Ghosh MK* (2014). HAUSP, a novel deubiquitinase for Rb – MDM2 the critical regulator.FEBS Journal 281: 3061–3078.
  9. Mandal T, Bhowmik A, Chatterjee A, Chatterjee U, Chatterjee S and Ghosh MK* (2014).Reduced phosphorylation of Stat3 at Ser-727 mediated by Casein Kinase 2 – Protein Phosphatase 2A enhances Stat3 Tyr-705 induced tumorigenic potential of glioma cells. Cellular Signaling 26: 1725-1734.
  10. Chatterjee A, Chatterjee U and Ghosh MK* (2013) Activation of protein kinase CK2 attenuates FOXO3a functioning in a PML-dependent manner: implications in human Prostate Cancer. Cell Death Dis. 4: e543.
  11. Bhowmik A, Das N, Pal U, Mandal M, Bhattacharya B, Sarkar M, Jaisankar P, Maiti NC, Ghosh MK* (2013). 2,29-Diphenyl-3,3′-Diindolylmethane: A Potent Compound Induces Apoptosis in Breast Cancer Cells by Inhibiting EGFR Pathway. PLoS One 8: e59798.
  12. Paul I, Ahmed F, Bhowmik A, Deb S and Ghosh MK* (2013). The Ubiquitin Ligase CHIP Regulates c-Myc Stability and Transcriptional Activity. Oncogene 32: 1284-95.
  13. Ahmed F, Deb S, Paul I, Mandal T, Chatterjee A and Ghosh MK* (2012). Stability and transcriptional activity of PTEN is controlled by E3 ubiquitin ligase CHIP. J Biol Chem. 287: 15996–16006.
  14. Naidu GKK, Mandal T, Chatterjee A, Sarkar M, Bhattacharya S, Chatterjee U and Ghosh MK* (2012). Crosstalk between Wnt/β-catenin and EGFR signaling is negatively controlled by GSK3β in prostate cancer. J Biol Chem. 287: 18287-96.