Ramachandran Rashmi

TL;DR: This review describes the mechanisms of curcumin-induced apoptosis currently known, and suggests several potential strategies that include down-regulation of antiapoptotic proteins by antisense oligonucleotides, use of proAPoptotic peptides and combination therapy, and other novel approaches against chemoresistant tumors.

TL;DR: In this paper, mild heat treatment induced the expression of heat shock protein-70 (hsp70), hsp90 and hsp27 in two human colon cancer cell lines, one derived from primary tumor, SW480, and the other derived from the secondary lymph node tissue, SW620, of the same patient.

TL;DR: The results from this study suggest that caspase-2 activation occurs upstream of mitochondria in resveratrol-treated cells, and the contribution of both Bax and Bak in mediating cell death induced by resver atrol and the existence of Bax/Bak-independent cell death possibly through casp enzyme-8- or caspasing-2-mediated mitochondria-independent downstream caspases.

TL;DR: The present study demonstrates the potential of hsp70 in protecting SW480 cells from curcumin-induced apoptosis and highlights that silencing the expression of hSp70 is an effective approach to augment curcuming-based therapy in cancers that are resistant due to h Sp70 expression.

TL;DR: The present study demonstrates the role of Bax but not Bak as a critical regulator of curcumin-induced apoptosis and implies the potential of targeting antiapoptotic proteins like Bcl-XL or overexpression of proapoptosis proteins like Smac as interventional approaches to deal with Bax-deficient chemo-resistant cancers for cur cumin-based therapy.