I am a Cell and Molecular Biologist working on the signal transduction mechanism of the evolutionarily conserved cellular process of autophagy in conjunction with the hyaladherin named, Hyaluronan-binding protein 1 (HABP1/p32/gC1qR).
My Doctoral and initial Post-Doctoral studies focussed towards unraveling the cellular dynamics of HABP1, the multifunctional human protein identified by our lab and implicated in several cellular functions and diseases; in cancer progression and metastasis. These work helped towards proving, that the elevated expression of HABP1 undoubtedly leads to enhanced HA synthesis, HA cable formation modifying the tumor potency in HepG2 cells. From my work on autophagy in the fibroblasts and hepatocarcinoma cell lines, I was able to establish a link between ectopic expression of HABP1, ROS generation and the homeostatic mechanism of autophagy, which is an associated phenomena during cancer progression.
PhD in Cell and Molecular Biology/Cancer Biology, Biochemistry & Toxicology Laboratory, School of Environmental Sciences, Jawaharlal Nehru University (New Delhi, 2012)
M.Sc in Environmental Sciences (Biology Group, Specialization in Cell and Molecular Biology, Environmental Toxicology), School of Environmental Sciences, Jawaharlal Nehru University (New Delhi, 2005)
B.Sc in Zoology Honours, Presidency College, Calcutta University (Kolkata, 2003)
Assistant Professor, Institute of Health Sciences (erstwhile School of Biotechnology), Presidency University, Kolkata (01st August, 2019 onwards)
Assistant Professor, Department of Life Sciences, Presidency University, Kolkata (25th March 2019 to 01st August, 2019)
Young Scientist, Start-up Research Grant awarded by Science and Engineering Research Board (SERB), DST (25th Feb, 2016 to 24th March, 2019), Molecular Endocrinology Laboratory, Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi
Senior Research Associate, under Scientists’ Pool Scheme of Council of Scientific and Industrial Research (11th June, 2014 to 24th Feb, 2016), Biochemistry and Toxicology Laboratory, School of Environmental Sciences, Jawaharlal Nehru University, New Delhi
Research Associate, (July 3, 2012 to April 2, 2014), Biochemistry and Toxicology Laboratory, School of Environmental Sciences, Jawaharlal Nehru University, New Delhi
CSIR/UGC NET-JRF (National Eligibility Test-Junior Research Fellowship) examination, Government of India (2005) in Life Sciences [JRF- Jan,2006 to Dec, 2007, SRF- Jan, 2008 to Dec, 2010].
Awarded NTSE scholarship (National Talent Search Examination) conducted by NCERT, India (1998).
Research / Administrative Experience+
1. Young Scientist, Start-up Research Grant awarded by Science and Engineering Research Board (SERB), DST , (2016 to 2019), Molecular Endocrinology Laboratory, Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, India
Project Title: “An insight into the molecular dynamics of Polycystic Ovarian Syndrome (PCOS) in conjunction to autophagy and HABP1 expression”
Summary of work done:
Polycystic ovarian (PCO) rat model generated by using the anti-progestogen RU486/mifepristone, histologically shows presence of numerous follicular cysts apart from several follicles lacking normal COC and intact apex. Observations imply impairment of normal folliculogenesis upon incidence of autophagy, resulting in polycystic ovarian morphology.
2. Senior Research Associate, under Scientists’ Pool Scheme of Council of Scientific and Industrial Research, (2014 to 2016), Biochemistry & Toxicology Laboratory, School of Environmental Sciences, Jawaharlal Nehru University, New Delhi, India
Project Title: “To elucidate HABP1 interactive proteins in HABP1 overexpressing HepG2 cells leading to increased tumor potency”
Summary of work done:
The study divulged that, splicing factors and reported oncogenes, SF2/SRSF1 and hnRNPA1 are upregulated in the HABP1 overexpressing HepG2 (HepR21) as compared to the parent HepG2 cells (Saha et al, 2018). SRSF1 reported to induce the mTORC1 pathway regulating cell survivability might have a role in downregulating autophagic machinery and decreased proteolysis by activation of mTORC1 pathway in HepR21. HepR21 cells were observed to have decreased tumor potency upon induction of autophagy by way of increased generation of ROS through depletion of HA levels only (Saha et al, 2014). It was very appealing to elucidate the signalling mechanism behind the upregulated HAS2 and HA levels. Interestingly, downregulation of HAS2 leading to declined HA levels resulted in diminished expression of the aforementioned oncogenes SRSF1 and hnRNPA1, indicating a regulatory role of endogenous HA (Saha et al, 2018).
3. Research Associate, in the DBT sponsored project, 2012 to 2014
Project Title: “Functional Role of cell surface Hyaluronan-binding Protein 1 (HABP1): Implication in cancer metastasis”
Summary of work done:
HABP1 overexpression in the redox insensitive HepG2 cells (HepR21) reportedly results in, cell surface localization of HABP1 with no excess ROS generation, cellular stress and apoptosis. Rather it induced enhanced cell growth and proliferation over longer periods with higher endogenous HA levels and intercellular HA cables (Kaul et al, 2012). Presumably, the surface localization of HABP1 in this stable transformant (HepR21) plays a significant part in the higher tumorigenic potential; evident from the increased survival rate in low serum condition, a shift towards anchorage independent growth and enhanced cell adhesion. This work has been further translated into 3D, using silk fibroin based three dimensional culture system and the increased tumor potency of HepR21 has been confirmed (Kundu and Saha et al, 2013). The increased tumor potency is correlated with inhibition of autophagic vacuole formation, low serum requirement, increased cell adhesion, downregulated expression of tumor suppressor, PTEN. Hyaluronan synthase (HAS) inhibitor and the anti-carcinogenic drug, 4-MU reverts these changes with decreased tumor potency and elevated expression of tumor suppressor protein, PTEN, Beclin1 and increased autophagic vacuole formation (Saha et al, 2014). Thus, sub-cellular HABP1 localization and its interaction with HA play a vital role in regulating autophagy and in turn tumor potency.
1. Superintendent, Presidency University Girl's Hostel, from June, 2020 till date.
2. Assistant Superintendent, Presidency University Girls Hostel, from April, 2019 till June, 2020.
3.. Member of Post graduate Research Advisory Committee (PRAC) for M.Sc. in Biotechnology courses, School of Biotechnology, Presidency University, from August, 2019.
4. Member of working committee for Instrumentation Facility, Institute of Health Sciences, (erstwhile School of Biotechnology, Presidency University), from August, 2019.
Teaching / Other Experience+
1. Postgraduate course on Molecular Biology and Cell Biology, Host-Microbiome Interaction, Environmental Biotechnology etc at Institute of Health Sciences (erstwhile School of Biotechnology), Presidency University, Kolkata
2. Postgraduate practical course on Molecular Biology Techniques, Environmental Biotechnology etc.
3. Undergraduate course (2nd year, CBCS students) on Public Health and Management
4. Undergraduate Course (First Year Students across all streams) on Ability Enhancement Compulsory Course (AECC- Environment Studies)
Post Graduate Supervision+
1. Ms. Abhipsha Ray (Registered PhD Scholar)
2. Ms. Nabanita Jotdar (M.Sc Dissertation Student)
1. Paramita Saha #, Sudhir Kumar, Kasturi Datta, Rakesh K Tyagi #. "Upsurge in autophagy, associated with mifepristone-treated polycystic ovarian condition, is reversed upon thymoquinone treatment". J Steroid Biochem Mol Biol, 2021 (Accepted) [ # Co-Corresponding author]
2. Kunwar Somesh Vikramdeo*, Paramita Saha*, Shubhra Dutta, Naveen Kumar, Anindya Roy Chowdhury, Sudhir Kumar, Rakesh K Tyagi, Ilora Ghosh*, Kasturi Datta. “Hyaluronan-binding protein 1 (HABP1) overexpression triggers induction of senescence in fibroblast cells”. Cell Biology International, 2020: doi: 10.1002/cbin.11326. [* KSV and PS have contributed equally]
3. Paramita Saha, Kasturi Datta. “Multifunctional Multicompartmental Hyaluronan binding-protein 1 (HABP1/p32/gC1qR): Implication in Cancer Progression and Metastasis”. Oncotarget, 2018, 9(12): 10784-10807. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5828189/
4. Paramita Saha, Rachna Kaul, Kasturi Datta. “Human gene encoding hyaluronan-binding protein 1 (HABP1/p32/gC1qR): Involvement in signaling cascade”. Nucleus (India), 2017, 60(2):221-226. doi:10.1007/s13237-017-0207-6. https://link.springer.com/article/10.1007/s13237-017-0207-6
5. Deepa Ruhela, Mohan Kamthan, Paramita Saha, Subeer Majumdar, Kasturi Datta, M Abdin, Asis Datta. "In vivo role of Candida albicans β-hexosaminidase (HEX1) in carbon scavenging". MicrobiologyOpen (Wiley Online), 2015, 4(5):730-42. https://www.ncbi.nlm.nih.gov/pubmed/26177944
6. Paramita Saha, Ilora Ghosh, Kasturi Datta. “Increased Hyaluronan Levels in HABP1/p32/gC1qR Overexpressing HepG2 Cells Inhibit Autophagic Vacuolation Regulating Tumor Potency”. PLoS ONE, 2014, 9(7):e103208. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4111551/
7. Paramita Saha, Anindya Roy Chowdhury, Shubhra Dutta, Soumya Chatterjee, Ilora Ghosh and Kasturi Datta. “Autophagic Vacuolation Induced by Excess ROS Generation in HABP1/p32/gC1qR Overexpressing Fibroblasts and its Reversal by Polymeric Hyaluronan”. PLoS ONE, 2013, Vol.8, Issue 10, e78131. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799741/
8. Banani Kundu*, Paramita Saha*, Kasturi Datta, S. C. Kundu. “Silk fibroin based hepatocarcinoma model: A 3D tool to evaluate transformation efficacy and drug response in Hyaluronan-binding protein 1 (HABP1) overexpressed HepG2 cells”. Biomaterials, 2013, Vol. 34, Issue 37, pp. 9462-9474. *BK and PS have contributed equally. https://www.ncbi.nlm.nih.gov/pubmed/24016853
9. Rachna Kaul, Paramita Saha, Mallampati Saradhi, L.A. Ramachandra Prasad, Soumya Chatterjee, Ilora Ghosh, Rakesh K. Tyagi and Kasturi Datta. “Overexpression of Hyaluronan Binding Protein 1 (HABP1/p32/gC1qR) in HepG2 cell leads to increased hyaluronan synthesis and cell proliferation by upregulation of cyclin D1 in AKT-dependent pathway”. Journal of Biological Chemistry, 2012, Vol. 287, No. 23, pp. 19750–19764. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366008/
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