Autophagy, especially macroautophagy is specifically reported to be a cellular survival strategy under drug stress. We are interested in understanding signaling molecules regulating autophagy upon chemo-therapeutic stress. We have also developed drug resistant cell lines and tracked regulation of autophagy during such acquisition of resistance. Simultaneously, alteration in developmentally active signaling pathways is analyzed and investigated for their contribution in regulating autophagy. Regulation of Hippo signaling pathway components under drug stress is currently investigated.
The tumor cells are invariably surrounded by an inflammatory niche. Thus, the stromal components are not just active bystanders in the pathogenesis of solid tumors, but one which play an active role in HCC progression. The tumor microenvironment serves as an innate resistance niche for chemotherapy assault and a physiological barrier against therapy. Hence, in our lab we are analyzing the crosstalk between stromal cells and tumor cells, with special emphasis on role of cytokines and growth factors.
Traditional cancer therapy uses highly cytotoxic drugs as chemotherapy. To reduce the off-target toxicity nanotechnology based platforms have emerged as attractive tools in cancer therapy. The nanoparticles can home into the tumor efficiently by using unique leaky vasculature by enhanced permeability and retention effect. Inspired by the need of developing novel biocompatible and biodegradable nanoplatform, the aim of our study is to analyze versatile nanoparticulate compounds for drug delivery and therapy. In collaboration, we are currently in the process of identifying/analyzing the therapeutic effect of nano-particulate drugs/compounds in resistant cancer cells.
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 mutants bestow cancer cells with chemo-resistant properties has not been extensively studied and deserves research intervention. In our lab, our primary objective is therefore to investigate novel molecular mechanisms of mut-p53-mediated chemo-resistance.