About the Faculty

Dr. Chowdhury completed his Master degree from Calcutta University (2001), and PhD (CSIR-NET 2003) from Jadavpur University (2009). He then joined Massachusetts Institute of Technology (MIT), USA, Department of Bio-engineering, as a post doctoral researcher in 2009. At Wogan lab, MIT he studied the myriad set of genetic events following Nitric Oxide (NO) exposure; his project extended from understanding the effects of NO-induced post translational modifications to its cancer promoting effect and also its role in cell death mechanisms like, Autophagy. In Oct 2012 he joined BITS Pilani as an Assistant Professor in Dept of Bio-Sciences. At BITS Pilani he is primarily involved in understanding the molecular signature of cancer cells surviving drug stress. 

Current Research Interest:

Overall Goal: Understanding Adaptive Drug Refractory Startegies of Tumor Cells

Our research team is involved in understanding the diverse molecular mechanisms or adaptations of tumor cells contributing to drug tolerance and resistance. In this regard, the following aspects are investigated:

1. Characterizing signaling and epigenetic adaptations of tumor cells upon drug stress (ICMR Funded): A toxic drug pressure often results in survival of a very small population of transitorily non-dividing tumor cells that eventually attain proliferative potential to re-populate tumor. Our research is devoted towards understanding the epigenetic signatures of these 'tolerant cells' that serve as a pool of resilient cells re-establishing tumor population. Herein, we have observed dynamic alteration in histone marks upon drug stress. In this regard, our primary interest is in identifying the role of Histone Demethylases (KDMs). Their functional implications in resistance and immune evasion are investigated. Overall, the understanding of the adaptive strategies of tumor cells upon drug pressure is directed towards identification of probable therapeutic targets preventing drug tolerance, resistance and hence associated recurrence of cancer. 
2. Understanding the role of autophagy during drug stress: The cellular homeostatic process, autophagy has often been implicated in hindering drug sensitivity. However, the precise mechanism- of regulation of autophagy and the latter itself controlling cellular survival under drug pressure is poorly understood. Herein, we monitor autophagy after differential drug pressure in tumor cells. Thereafter, coupled with in silico analysis we identify signaling molecules/proteins regulating or having a crosstalk with autophagy. We further explore how modulating the identified molecules/autophagy can enhance chemotherapeutic sensitivity. In this context, we are further interested to explore the role of selective autophagy-mitophagy upon drug stress.
3. Exploring the role of master transcription regulator- YAP and LIM protein-Ajuba in drug resistance (DBT Builder funded): Alteration in expression of developmentally active signaling pathways is a hallmark of cancer and associated drug resistance. Currently we are exploring the role of Hippo signaling pathway components, like YAP under drug stress and its crosstalk with cellular adaptive strategies. Further, as part of DBT Builder project, we are exploring the regulation and role of LIM-family protein-Ajuba in drug tolerance.
4. Analyzing role of high glucose in tumor drug resistance (SERB funded): Hyperglycemic conditions are often positively correlated with progression of cancer, including pancreatic cancer. Especially, hyperglycemia is known to be associated with drug resistance as well. However, the precise mechanism of how hyperglycemia has an impact on drug resistance is poorly characterized. In this project, we explore the role of specific long non-coding RNAs (lncRNAs) de-regulated under hyperglycemic conditions. Through genetic manipulation, their role in resistance through rewiring tissue metabolism is thereafter investigated. Moving ahead, we explore whether these lncRNAs regulate chromatin dynamics under high glucose conditions thus controlling selective transcription of genes.
5. Role of GOF p53 in drug resistance (DBT funded): p53 is one of the most important tumor suppressors; however, in over half of human cancers, p53 is inactivated due to mutations. Mutant p53 possess distinctive activities of their own, often not present in the wild-type p53 protein. This endows the mutant proteins with activities that contribute to tumor progression and chemo-resistance. However, the mechanism by which these mutant cancer cells can be sensitized has not been extensively studied. In this project, we explore the potential of regulation of protein homeostasis as a therapeutic strategy to attenuate GOF-p53 mediated effect on drug resistance and survival.
6. Platelet autophagy and thrombosis (LSRB funded): This project explores the role of autophagy and selective autophagy like, mitophagy in low oxygen induced platelet activation and thrombosis. The objective of this project is directed towards reducing and designing an appropriate therapy to prevent hypoxia induced thrombosis in people moving to high altitudes, especially, the soldiers. In parallel we are also investigating platelet and circulating tumor cell (CTC) interaction and its crosstalk with endothelial cells.