| Literature DB >> 32575867 |
Sandy Anania1,2, Raphaël Peiffer1,2, Gilles Rademaker1,2, Alexandre Hego3, Marc Thiry4, Louise Deldicque5, Marc Francaux5, Naïma Maloujahmoum1, Ferman Agirman1, Akeila Bellahcène1, Vincent Castronovo1, Olivier Peulen1,2.
Abstract
Pancreas ductal adenocarcinoma is one of the deadliest cancers where surgery remains the main survival factor. Mitochondria were described to be involved in tumor aggressiveness in several cancer types including pancreas cancer. We have previously reported that myoferlin controls mitochondrial structure and function, and demonstrated that myoferlin depletion disturbs the mitochondrial dynamics culminating in a mitochondrial fission. In order to unravel the mechanism underlying this observation, we explored the myoferlin localization in pancreatic cancer cells and showed a colocalization with the mitochondrial dynamic machinery element: mitofusin. This colocalization was confirmed in several pancreas cancer cell lines and in normal cell lines as well. Moreover, in pancreas cancer cell lines, it appeared that myoferlin interacted with mitofusin. These discoveries open-up new research avenues aiming at modulating mitofusin function in pancreas cancer.Entities:
Keywords: mitochondria; mitofusin; myoferlin; pancreas cancer
Year: 2020 PMID: 32575867 DOI: 10.3390/cancers12061643
Source DB: PubMed Journal: Cancers (Basel) ISSN: 2072-6694 Impact factor: 6.639