Kaushik Biswas
Bose Institute, Bose Institute - Centenary Campus, Cleveland Clinic, Indian Institute of Chemical Biology CSIR, University of Calcutta
About
Following my post graduation from the University of Calcutta in 1996, I joined the Indian Institute of Chemical Biology (IICB) and successfully completed my PhD in Life Sciences in 2000. After doing a brief post-doc in my parent lab, I joined the Lerner Research Institute at the Cleveland Clinic for my post-doctoral studies in the area of tumor-induced immune suppression, and its mechanism. In the year 2010, I joined Bose Institute, Kolkata as an Assistant Professor, and has been there since. In the year 2015, I was promoted to Associate Professor. During my stint as a Principal Investigator, I have taken an all round approach towards understanding the basis of aberrant ganglioside expression in various tumors as well as studying the consequence of such an abnormal expression in carcinogenesis. Gene silencing as well as molecular cloning and over-expression strategies were utilized to establish the potential role of tumor derived glycosphingolipids in migration as well as invasion of tumor cells. Gene expression profiling suggests a large number of differentially regulated gene sets (DRGs) in response to GM2-synthase knockdown and mechanistic studies reveal a critical role of the integrin signaling pathway to be involved in GM2 mediated tumor cell migration. With an aim to translate these in vitro findings in vivo, targeted genome editing technology by TALEN is used to define the functional role of GM2 in tumorigenesis. Studies indicate that GM2 is involved in epithelial-mesenchymal transition (EMT) by promoting anoikis resistance in tumors. Studies are under way to elucidate the mechanism of GM2 mediated EMT. Finally, I have initiated a study to find out the basis of over-expression of several ganglioside synthase genes in cancer, currently focusing on the regulation of GM2-synthase gene. Very recently, data from our lab showed that the GM2-synthase gene is epigenetically regulated in renal cell carcinoma (RCC or kidney cancer) which may well extend to other cancers as well. In this recent finding, we uncovered a novel mechanism regulating the expression of this oncogene, GM2-synthase at the transcriptional level. On a different note, we have very recently undertaken a collaborative study, to screen and identify potential anti-inflammatory compounds from natural sources, those by virtue of being anti-inflammatory may be able to protect against chronic inflammation induced disease pathogenesis, like cancer.
Employment
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Bose Institute Professor2020 - Present
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Bose Institute - Centenary Campus Associate Professor2015 - Present
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Bose Institute - Centenary Campus Assistant Professor2010 - 2015
Education
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Cleveland Clinic Post Doctoral2003 - 2010
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Indian Institute of Chemical Biology CSIR Post Doctoral2001 - 2003
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Indian Institute of Chemical Biology CSIR PhD1997 - 2001
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University of Calcutta MSc1994 - 1996
Projects & Funding
Projects & funding information is unavailable.
Publications (42)
- Ganglioside GM2 induces epithelial–mesenchymal transition (EMT) in cancer cells in a MEK/ERK/Egr1-dependent transcriptional program Save
- Identification of miR-615-5p/ID1 axis crucial in the pathogenesis of pancreatic ductal adenocarcinoma (PDAC) Save
- dCas9 Targeted Proteome Profiling Reveals p300‐Mediated Reciprocal Regulation of SMAD and SP1 as a Driver of GM2‐synthase Transcription in Renal Cell Carcinoma Save
- Non-Canonical Targets of MicroRNAs: Role in Transcriptional Regulation, Disease Pathogenesis and Potential for Therapeutic Targets Save
- Multi-dimensional role of gangliosides in modulating cancer hallmarks and their prospects in targeted cancer therapy. Save
- Eriodictyol mediated selective targeting of the TNFR1/FADD/TRADD axis in cancer cells induce apoptosis and inhibit tumor progression and metastasis. Save
- Ricinus communis L. fruit extract inhibits migration/invasion, induces apoptosis in breast cancer cells and arrests tumor progression in vivo Save
- Elevated histone H3 acetylation and loss of the Sp1–HDAC1 complex de-repress the GM2-synthase gene in renal cell carcinoma Save
- Regulation of monoamine oxidase A (MAO-A) expression, activity, and function in IL-13–stimulated monocytes and A549 lung carcinoma cells Save
- Inhibition of cancer progression by a novel trans-stilbene derivative through disruption of microtubule dynamics, driving G2/M arrest, and p53-dependent apoptosis Save