MSc, BSc

Meera Venugopal is currently a Research Scholar at the School of Biotechnology. She received his masters in Biotechnology from Amrita Vishwa Vidyapeetham, Amritapuri in 2012. She is currently pursuing her PhD in Biotechnology at Cell Biology Lab.


  • M. Sc. Biotechnology, Amrita Vishwa Vidyapeetham (2012)
  • B. Sc. Microbiology, Amrita Vishwa Vidyapeetham (2010)


  • Qualified CSIR-UGC-NET for Lectureship, 2011
  • Qualified GATE exam, 2012
  • 1st rank in B. Sc. Microbiology (2007-2010) from Amrita Vishwa Vidyapeetham


Publication Type: Journal Article

Year of Publication Title


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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