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Parkin in Parkinson’s Disease and Cancer: a Double-Edged Sword

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Abstract

Parkin for more than a decade has been portrayed as a neuroprotector gene is now increasingly emerging as a multifaceted gene that can exert entirely opposite effects i.e., both cell proliferation and apoptosis. Parkinson’s disease, a neurological disease, progresses due to excess in cell death, while, in case of cancer, cell death normally fails to occur. Parkin, an E3 ubiquitin ligase, was first identified as a gene implicated in autosomal recessive juvenile Parkinsonism, but several evidences indicate that Parkin is a tumor suppressor gene, involved in a variety of cancers. It is hard to imagine that two entirely different classes of disease, like cancer and Parkinson’s disease, can converge at a critical point attributable to a single gene, Parkin. This mysterious and hidden connection may prove a boon in disguise and has raised hopes that studying the biology of one disease may help to identify novel targets of therapy for the other. In this Parkinson’s disease–cancer story, if the detail of Parkin pathway is unraveled and gaps in the storyline are properly filled up, we may end getting an entirely new therapeutic option. This review mainly highlights the recent literature which suggests how Parkin gene regulates the various hallmarks of both the Parkinson’s disease and cancer.

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This review was supported by the grant from the Department of Science and Technology (DST).

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Wahabi, K., Perwez, A. & Rizvi, M.A. Parkin in Parkinson’s Disease and Cancer: a Double-Edged Sword. Mol Neurobiol 55, 6788–6800 (2018). https://doi.org/10.1007/s12035-018-0879-1

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