Mitophagy and Bip–PERK–eIF2α–ATF4 Axis‐Mediated ER Stress Mediate Miriplatin‐Loaded Liposome's Anti‐Colorectal Cancer Action
Cong Zhao, Yuhan Qiu, Xiaowei Wang, Mengyan Wang, Li Liu, Xiaojun Zhao, Zixiang Gao, Rongguang Shao, Guimin Xia, Wuli Zhao
TL;DR
A drug-loaded liposome fights breast cancer by triggering cell stress and death through specific pathways.
Contribution
The study reveals a new mechanism of anti-cancer action involving mitophagy and ER stress pathways.
Findings
Miriplatin-loaded liposomes induce mitophagy via lysosome-mitochondria fusion.
ER stress is activated through the Bip–PERK–eIF2α–ATF4 axis, leading to apoptosis.
The treatment shows anti-breast cancer effects via caveolin-mediated endocytosis.
Abstract
LMPt enters the cell mainly through caveolin‐mediated endocytosis, and then fuses with endosomes and lysosomes to deliver MPt to mitochondria and the endoplasmic reticulum to induce mitophagy based on the fusion of lysosomes and mitochondria, and endoplasmic reticulum stress and subsequent apoptosis via the Bip–PERK–eIF2α–ATF4 axis to exert an anti‐breast cancer effect.
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Taxonomy
TopicsAutophagy in Disease and Therapy · Endoplasmic Reticulum Stress and Disease · Caveolin-1 and cellular processes