Qualification: 
Ph.D
gkumar@am.amrita.edu

Dr. Kumar obtained her Ph.D from the University of Tennessee, Memphis, USA, where she elucidated the structure-function activity of fadL, a bacterial Long Chain Fatty Acid binding protein. Following her Ph.D, Dr. Kumar did her post-doctoral studies under Dr. Neil Nathanson, at the University of Washington, Seattle, USA, on the regulation of Muscarinic Acetylcholine Receptor (mAChR). She was subsequently associated with Ceptyr Inc., a Biotech company where she worked in the High Throughput Screening (HTS) division that focused on developing drugs against Diabetes.

Dr. Kumar is currently an Professor at the School of Biotechnology, Amrita Vishwa Vidyapeetham, where her research focuses on identification and characterization of Natural Product Lead molecules and understanding their role in:

  • Regulating Matrix Metalloproteinases and oncogenic signaling systems and elucidating the molecular mechanisms underlying this process
  • Modulating the complex processes involved in wound healing
  • Pathogenesis and virulence with specific emphasis on Quorum Sensing
  • Cardio-protection to enable their use in combination therapies
  • Regulating Inflammasomes and the inflammatory signaling cascades in disease states

Ongoing research interests also include understanding the role played by miRNAs in regulating oncogenesis and exploring the potential of their use independently, or in combination therapies, along with Natural Products. 

Research Support :

Grant funded in the Science Research Scheme (SRS),(2014) Kerala State Council for Science, Technology and Environment, Govt. Of Kerala:  Elucidating the Molecular Mechanisms of Anacardic Acid Mediated Regulation of Matrix Metalloproteinases in Cancer

Positions and Honours :

  • Research Fellow, 1994-1996, MDS Pharma, Seattle, Washington, USA.
  • Research Scientist, 1996 - 2004, Ceptyr Pharmaceuticals Inc., Seattle, Washington, USA.
  • Professor, 2007-Current, Amrita School of Biotechnology
  • Organizing and Program committee member, International Conference on Biotechnology for Innovative Applications (Amrita BioQuest  2013), Amritapuri, India.

Teaching

Publications

Publication Type: Journal Article

Year of Publication Title

2019

Damu Sunilkumar, Drishya G., Chandrasekharan, A., Shaji, S. K., Chinchu Bose, Jossart, J., J. Jefferson P. Perry, Dr. Nandita Mishra, Dr. Geetha Kumar, and Dr. Bipin G. Nair, “Oxyresveratrol drives caspase-independent apoptosis-like cell death in MDA-MB-231 breast cancer cells through the induction of ROS.”, Biochem Pharmacol, p. 113724, 2019.[Abstract]


Earlier studies from our laboratory have demonstrated that Oxyresveratrol (OXY), a hydroxyl-substituted stilbene, exhibits potent inhibition of human melanoma cell proliferation. The present study defines a cytotoxic effect of OXY on the highly chemo-resistant, triple-negative human breast cancer cell line MDA-MB-231. OXY-mediated cell death resulted in accumulation of cells at the sub-G1 phase of the cell cycle, induced chromatin condensation, DNA fragmentation, phosphatidylserine externalization and PARP cleavage, indicative of apoptosis. Interestingly, morphology and cell viability studies with the pan-caspase inhibitor, QVD-OPH revealed that OXY-induced cell death was caspase-independent.Docking studies also showed that OXY can bind to the S1 site of caspase-3, and could also exert an inhibitory effect on this executioner caspase. The immunoblot analysis demonstrating the absence of caspase cleavage during cell death further confirmed these findings. OXY was also observed to induce the production of reactive oxygen species, which caused the depolarization of the mitochondrial membrane resulting in translocation of Apoptosis Inducing Factor (AIF) into the nucleus. Pretreatment of the cells with N-Acetyl Cysteine antioxidant prevented cell death resulting from OXY treatment. Thus, OXY initiates ROS-mediated, apoptosis-like cell death, involving mitochondrial membrane depolarization, translocation of AIF into the nucleus, and DNA fragmentation, resulting in caspase-independent cell death in MDA-MB-231 cells. The cytotoxicity manifested by OXY was also observed in 3D cell culture models and primary cells, thereby providing a basis for the utilization of OXY as a novel template for the future design of anticancer therapeutics.

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2016

Dr. Jyotsna Nambiar, Chinchu Bose, Meera Venugopal, Dr. Asoke Banerji, T. B. Patel, Dr. Geetha Kumar, and Dr. Bipin G. Nair, “Anacardic acid inhibits gelatinases through the regulation of Spry2, MMP-14, EMMPRIN and RECK”, Experimental Cell Research, vol. 349, pp. 139-151, 2016.[Abstract]


Earlier studies from our laboratory have identified Anacardic acid (AA) as a potent inhibitor of gelatinases (MMP-2 and 9), which are over-expressed in a wide variety of cancers (Omanakuttan et al., 2012). Disruption of the finely tuned matrix metalloproteinase (MMP) activator/inhibitor balance plays a decisive role in determining the fate of the cell. The present study demonstrates for the first time, that in addition to regulating the expression as well as activity of gelatinases, AA also inhibits the expression of its endogenous activators like MMP-14 and Extracellular Matrix MetalloProteinase Inducer (EMMPRIN) and induces the expression of its endogenous inhibitor, REversion-inducing Cysteine-rich protein with Kazal motifs (RECK). In addition to modulating gelatinases, AA also inhibits the expression of various components of the Epidermal Growth Factor (EGF) pathway like EGF, Protein Kinase B (Akt) and Mitogen-activated protein kinases (MAPK). Furthermore, AA also activates the expression of Sprouty 2 (Spry2), a negative regulator of EGF pathway, and silencing Spry2 results in up-regulation of expression of gelatinases as well as MMP-14. The present study thus elucidates a novel mechanism of action of AA and provides a strong basis for utilizing this molecule as a template for cancer therapeutics.

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PDF iconanacardic-acid-inhibits-gelatinases-through-the-regulation-of-spry-2-mmp-14-emmprin-and-reck-11october2016.pdf

2015

Dr. Jyotsna Nambiar, Dr. Geetha Kumar, Sanjana S. R., Gorantla S. N., Lankalapalli R. S., and Dr. Bipin G. Nair, “A Novel2-Alkoxy-3, 5-Dihydroxypyridine Mediated Regulation of Gelatinases”, International Journal of Pharma and Bio Sciences, vol. 6, pp. 779-788, 2015.

2001

L. S. Nadler, Dr. Geetha Kumar, and Nathanson, N. M., “Identification of a basolateral sorting signal for the M3 muscarinic acetylcholine receptor in Madin-Darby canine kidney cells”, Journal of Biological Chemistry, vol. 276, pp. 10539–10547, 2001.

1999

L. S. Nadler, Dr. Geetha Kumar, Hinds, T. R., Migeon, J. C., and Nathanson, N. M., “Asymmetric distribution of muscarinic acetylcholine receptors in Madin-Darby canine kidney cells”, American Journal of Physiology-Cell Physiology, vol. 277, pp. C1220–C1228, 1999.

1989

V. G. Chinchar, Turner, L. A., and Dr. Geetha Kumar, “Hemin and cyclic AMP stimulate message-dependent translation in lysates from Friend erythroleukemia cells.”, Experimental hematology, vol. 17, pp. 405–410, 1989.

Publication Type: Conference Paper

Year of Publication Title

2017

Sanu K Shaji, Damu Sunilkumar, Drishya G., Dr. Geetha Kumar, and Dr. Bipin G. Nair, “MicroRNA-491 functions to down regulate both matrix metalloproteinase-9 and epidermal growth factor receptor expression and inhibit cell migration in MDA-MB-231 triple negative breast cancer cells (Poster)”, in 27th Swadeshi Science Congress, Amritapuri, 2017.

2015

A. Omanakuttan, Dr. Geetha Kumar, and Dr. Bipin G. Nair, “Ecdysterone Mediates Wound Healing in a Nitric Oxide Dependent Manner in 3T3L1 Fibroblasts.”, in The XXXIX All India Cell Biology Conference , 2015.[Abstract]


Ecdysteroids are insect moulting hormones which are structurally different from mammalian steroids, but have been shown to have several beneficial effects in mammals. Ecdysterone is known to enhance wound healing in rabbits by a faster granulation tissue formation and epithelial cell proliferation. In this study, we focused our efforts on elucidating the molecular mechanism involved in Ecdysterone mediated wound healing. In order to achieve this, we employed an in vitro wound healing assay using 3T3L1 cells treated with Ecdysterone, isolated from Sesuvium portulacastrum. The assay demonstrated that Ecdysterone enhanced in vitro wound healing activity in a dose dependent manner. Further studies demonstrated that Ecdysterone enhanced cell proliferation and cell migration in a nitric oxide dependent manner. Additionally, fluorescence studies with DAF FM diacetate, a specific indicator for nitric oxide, demonstrated that Ecdysterone enhances nitric oxide (NO) production in a dose dependent manner through activation of Nitric oxide Synthase (NOS). These results demonstrate that Ecdysterone can enhance the wound healing process in a nitric oxide (NO) dependent manner

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Publication Type: Patent

Year of Publication Title

2012

E. Schaefer, Dr. Bipin G. Nair, and Dr. Geetha Kumar, “Key pad for Medical Devices”, 2012.

Patents:

Year Title
2012 Key pad for Medical Devices, Design No. 244105, The Patent Office, Government of India_ Certificate of Registration of Design, 2012.