Targeting AMPK in cancer therapy: Alteration of lipid synthesis pathways
Thursday, March 1, 2018
MBG Conference Hall
Assoc. Prof. Elif Damla ARISAN
Department of Molecular Biology and Genetics, KulturUniversity
Elif Damla Arisan is Associate Professor at Istanbul Kultur University, Department of Molecular Biology and Genetics. She is founding member of the department since 2006.
She has received her PhD degree (2009) at Biological Sciences and Bioengineering Program at Sabanci University. Her research focus is molecular cell biology, especially identification of the role of cell decision pathways and clarification of novel therapeutic targets in different in vitro cancer cells and model organisms as C. elegans. Dr. Arisan authored over 40 peer-reviewed manuscripts. She has received a number of grants from TUBITAK, international COST actions and has awards from different institutions. Dr Arisan is the founder of DAPGenomics at Istanbul Technical University Technopark at 2017 and got support from Ministry of Science and Technology on development of genomic testing panels about maternal milk and nutrition relationship under Nutrilena brand name.
Cancer is associated with obesity, which is common health problem for aging populations worldwide. It is well established that obesity renders effect of drugs and lead to poor prognosis of disease via increasing fatty acid synthesis and cholesterol metabolism in cancer cells. Therefore, identification of potential therapeutic effect of anti-obesity drugs in the treatment of cancer cells through modulating lipogenesis and adipogenesis is an interesting study topic. One of the leading molecular target of these drugs is AMPK, a-well characterized kinase and a sensor mechanism for energy regulations in the cells. According to our findings, a lipase inhibitor Orlistat (Xenical, Roche) or celastrol, root extracts of Tripterygium wilfordii becomes critical in the treatment of cancer cells as anti-tumoral agents. As well as orlistat, celastrol mediated cell death is promising due activation of AMPK related upstream or downstream pathways in cancer cells. Supporting this finding, it was shown that AMPK is a critical target in aggressive forms of prostate cancer. Therefore, silencing or inactivation of AMPK in the androgen irresponsive prostate cancer cells might be critical in the treatment of aggressive prostate cancer. However, it is required to evaluate potential targets of lipase inhibitors in the absence or presence of AMPK. Therefore, targeting lipid metabolism-related enzymes in prostate cancer may offer new avenues for therapeutic approaches.