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 - mrinal.res@gmail.com / mrinalghosh@iicb.res.in


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

Fellow/RA
        1. Tapashi Mandal (SRF, CSIR) : tapashi.mondal@gmail.com
        2. Seemana Bhattacharya (SRF, CSIR) : seemana.bhattacharya@gmail.com
        3. Anirban Chatterjee (SRF, CSIR) : iam_anirban@hotmail.com
        4. Arijit Bhowmik (SRF, CSIR) : arijitbhoumik@gmail.com
        5. Nilanjana Das (SRF, CSIR) : nilanjana2008@gmail.com
        6. Moumita Sarkar (SRF, CSIR) : moumitasarkar.biology@gmail.com
        7. Syed Feroj Ahmed (SRF, UGC) : ferojahmeds@gmail.com
        8. Rajni Khan (JRF, UGC) : khanrajni@gmail.com
        9. Neerajana Datta (JRF, CSIR) : neerajana.datta@gmail.com
        10. Veenita Khare (JRF, UGC) : k.veenita@gmail.com
        11. Aroni Chatterjee (JRF, ICMR) : ronychatterjee88@gmail.com

Currently two positions are open for individuals with excellent academic credentials.
We encourage M.Sc. (life sciences) students with JRF award and MBBS/MD candidates interested in biomedical research to discuss the possibilities of joining our research team.  When contacting us please include your resume (including photo) and a brief statement of professional goals. Research experience in good academic Institutions like IISc, CCMB, NCCS, JNCSAR etc will also be encouraged.

List of important Research Articles (2012----)

Articles

  1. Bhattacharya S and Ghosh MK* (2014). HAUSP, a novel deubiquitinase for Rb – MDM2 the critical regulator.FEBS Journal. [DOI:10.1111/febs.12843].
  2. Dhar A et al., (2014). Simultaneous Inhibition of Key Growth Pathways in Melanoma Cells and Tumor Regression by a Designed Bidentate Constrained Helical Peptide. Biopolymers Peptide Science Journal [DOI: 10.1002/bip.22505].
  3. 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.
  4. 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.
  5. 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.
  6. De K et al., (2012). Synthesis, radiolabeling, and preclinical evaluation of a new octreotide analog for somatostatin receptor-positive tumor scintigraphy. J Peptide Science 18: 720-730.
  7. 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.
  8. Paul I, Ahmed SF, Bhowmik A, Deb S, Ghosh MK* (2012). The ubiquitin ligase CHIP regulates c-Myc stability and transcriptional activity. Oncogene 32(10):1284-95.
  9. 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

Reviews / Book Chapters

  1. Paul I and Ghosh MK*(2014). The E3 ligase CHIP: insights into its structure and  regulation. BioMed Res. Int. [DOI: org/10.1155/2014/918183].
  2. Bhattacharya S and Ghosh MK* (2014). Cell Death and Deubiquitinases: Perspectives in Cancer. BioMed Res. Int. [In press].
  3. 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 4 (11-12), 427-446.
  4. 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.

 

 
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Updated on 9th June 2014


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