Cancer Biology & Inflammatory Disorder Division

Dr. Mrinal Kanti Ghosh

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

Contact - /

Principal Scientist

Lab Website : Click Here

Current 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.

Names of the group members including regular staff with designation and research fellows

        1. G. Kiran Kr. Naidu (SRF, CSIR) :
        2. Tapashi Mandal (SRF, CSIR) :
        3. Seemana Bhattacharya (SRF, CSIR) :
        4. Anirban Chatterjee (SRF, CSIR) :
        5. Arijit Bhowmik (SRF, CSIR) :
        6. Nilanjana Das (SRF, CSIR) :
        7. Moumita Sarkar (SRF, CSIR) :
        8. Syed Feroj Ahmed (SRF, UGC) :
        9. Satamita Deb (SRF,CSIR) :
        10. Rajni Khan (JRF, UGC) :
        11. Neerajana Datta (JRF, CSIR) :
        12. Veenita Khare (JRF, UGC) :

List of important Research Articles (2011-13)

  1. Paul I, Bhattacharya S, Chatterjee A and Ghosh MK*(2013). Current Understanding on EGFR and Wnt/β-Catenin Signaling in Glioma and Their Possible Crosstalk. Genes & Cancer (In press).
  2. Ahmed SF and Ghosh MK *(2013). Post-Translational Regulation of PTEN and its Implication in Cancer. Chapter-2 of Book entitled "PTEN: Structure, Mechanism-of-Action, Role in Cell Signaling and Regulation" published by Nova Science Publishers, Inc.
  3. Bhowmik A, Das N, Pal U, Mandal M, Bhattacharya S, Sarkar M, Jaisankar P, Maiti NC and Ghosh MK* (2013). 2,2'-diphenyl-3,3'-diindolylmethane: A potent compound induces apoptosis in breast cancer cells by inhibiting EGFR pathway. PlosOne 8(3): e59798. doi:10.1371/journal.pone.0059798.
  4. Chatterjee A, Chatterjee U, Ghosh MK* (2013). Activation of Protein Kinase CK2 attenuates FOXO3a functioning in a PML dependent manner: implications in Human Prostate Cancer. Cell Death & Disease (2013) 4, e543; doi:10.1038/cddis.2013.63.
  5. De K, Bhowmik A, Behera A, Banerjee I, Ghosh MK and Misra M (2012). Synthesis, radiolabeling, and preclinical evaluation of a new octreotide analog for somatostatin receptor-positive tumor scintigraphy. J Peptide Science 18: 720-730.
  6. Guturi KK, Mandal T, Chatterjee A, Sarkar M, Bhattacharya S, Chatterjee U, Ghosh MK* (2012). Mechanism of β-catenin mediated transcriptional regulation of EGFR expression in GSK3β inactivated prostate cancer cells. J Biol Chem. 287:18287-18296.
  7. Paul I, Ahmed SF, Bhowmik A, Deb S, Ghosh MK* (2012). The ubiquitin ligase CHIP regulates c-Myc stability and transcriptional activity. Oncogene 1-12. PMID: 22543587
  8. Ahmed SF, Deb S, Paul I, Chatterjee A, Mandal T, Chatterjee U, Ghosh MK* (2012). The chaperone assisted E3 ligase CHIP targets PTEN for proteasomal degradation. J Biol Chem. 287:15996-6006
  9. Mondal S, Bandyopadhyay S, Ghosh MK, Mukhopadhyay S, Roy S & Mandal C (2011). Natural products: Promising resources for cancer drug discovery. Anticancer Agents Med Chem. 12: 49-75.
  10. Dazard JE, Zhang K, Sha J, Yasin O, Cai L, Nguyen C, Ghosh MK, Bongorno J and Harter ML* (2011). The dynamics of E1A in regulating networks and canonical pathways in quiescent cells. BMC Research Notes 2011, 4:160.

Other key publications:

  1. Sha J, Ghosh M.K†, Zhang K and Harter, ML (2010). E1A interacts with two opposing transcriptional pathways to induce quiescent cells into S phase. Journal of Virology 84:4050-9.
  2. Ghosh MK, Sharma P, Harbor PC, Rahaman SO and Haque SJ (2005). PI3K-AKT pathway negatively controls EGFR-dependent DNA-binding activity of Stat3 in glioblastoma multiforme cells. Oncogene, 24: 7290-300.
  3. Ghosh MK and Harter ML (2003). A viral mechanism for remodeling chromatin structure in Go cells. Molecular Cell, 12: 255-260.
  4. Chattopadhyay D, Ghosh MK, Mal A and Harter ML (2001). Inactivation of p21 by E1A leads to the induction of apoptosis in DNA-damaged cells. Journal of Virology, 75: 9844-9856.
  5. Mal A, Sturniolo M, Schiltz RL, Ghosh MK and Harter ML (2001). A role for histone deacetylase HDAC1 in modulating the transcriptional activity of MyoD: Inhibition of the myogenic program. EMBO. J., 20: 1739-1753.
  6. Mal A, D. Chattopadhyay, Ghosh MK, Poon RYC and Harter ML (2000). p21 and Retinoblastoma protein control the absence of DNA replication in terminally differentiated muscle cells. Journal of Cell Biology, 149: 281-292.
  7. Panda K, Chatterjee R, Ghosh MK, Chattopadhyay DJ and Chatterjee IB (1999). Vitamin C prevents cigarette smoke induced oxidative damage of proteins and increased proteolysis. Free Rad. & Biol. Med., 27: 1064-1079.

  [ contributed equally; *Corresponding author ]

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Updated on 11th March 2014

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