Cancer is a disease of uncontrolled proliferation which initially arises as a result of dysregulation in some gene candidates responsible for maintaining a normal cellular state. Some genes are suppressed with a concomitant increase in the expression of certain dormant ones. The former group constitutes the tumor suppressors while as the later- the oncogenes. Parkin a PARK 2 gene product is a potent tumor suppressor, has been well reported to be down regulated in many cancer types. Besides its tumor suppressor role, it regulates the redox state of the cell and recently it was reported to be an important factor in TP53 (a master tumor suppressor protein) mediated tumor suppression provides a clue about the role of Parkin in metabolic deregulation- an emerging hallmark of cancer! To this end, here we present that how Parkin is regulated under different environmental conditions and how it governs metabolic plasticity- glycolytic phenotype and hence cellular migration.

To conclude, the results show that Parkin differentially regulates metabolism by modulating certain potent marker candidates responsible for Warburg effect and associated carcinogenesis.

[MMA Rizvi is the corresponding author for this work.]

Note: This abstract was not presented at the meeting.

Citation Format: Zafar I. Bhat, Khalid Imtiyaz, M. Moshahid Rizvi. Interplay of Parkin, a 'tumor suppressor’ in metabolic deregulation of cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 5302.