Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC-1 cell apoptosis via activating the mROS-HtrA2/Omi pathways

Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC-1 cell apoptosis via activating the mROS-HtrA2/Omi pathways

Abstract Background Mitochondrial fragmentation drastically regulates the viability of pancreatic cancer through a poorly understood mechanism. The present study used erlotinib to activate mitochondrial fragmentation and then investigated the downstream events that occurred in response to mitochondr...

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Bibliographic Details
Main Authors: Jun Wan, Jie Cui, Lei Wang, Kunpeng Wu, Xiaoping Hong, Yulin Zou, Shuang Zhao, Hong Ke
Format: Article
Language:English
Published: BMC 2018-10-01
Series:Cancer Cell International
Subjects:
Erlotinib
Mitochondrial fragmentation
Mitochondrial apoptosis
mROS
HtrA2/Omi
Online Access:http://link.springer.com/article/10.1186/s12935-018-0665-1

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http://link.springer.com/article/10.1186/s12935-018-0665-1

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