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Mitofusin-2 triggers mitochondria Ca2+ influx from the endoplasmic reticulum to induce apoptosis in hepatocellular carcinoma cells.

Abstract：

:In previous studies, we confirmed that mitofusin-2 (Mfn2) induced apoptosis in hepatocellular carcinoma (HCC) cells. However, the exact molecular mechanism remained unclear. Mfn2 expressed lower in tumour tissues, compared with adjacent non-cancer tissues. Furthermore, Mfn2 immunostaining was very weak in HCC tissue (P < 0.05) and was significantly associated with tumour size and TNM stage (P = 0.038 and 0.040, respectively), and patients with HCC with lower Mfn2 expression had a poorer prognosis. Overexpression of Mfn2 induced HepG2 cells apoptosis, reduced the mitochondrial membrane potential (ΔΨm) and endoplasmic reticulum (ER) calcium ion (Ca(2+)) concentrations, and elevated intracellular reactive oxygen species (ROS) and mitochondrial Ca(2+) concentrations. However, when HepG2 cells overexpressing Mfn2 were treated with both heparin and RU360, there was no induction of apoptosis, decline in ΔΨm or ER Ca(2+), or increase in intracellular ROS or mitochondrial Ca(2+). We also found downregulation in the expression of mitochondrial calcium uptake1 and 2 (MICU1 and MICU2) in cells transfected with Adv-Mfn2. Thus, we confirmed that Mfn2 induced apoptosis in HCC cells by triggering influx of Ca(2+) into the mitochondria from the ER.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Wang W,Xie Q,Zhou X,Yao J,Zhu X,Huang P,Zhang L,Wei J,Xie H,Zhou L,Zheng S

doi

10.1016/j.canlet.2014.12.025

subject

Has Abstract

pub_date

2015-03-01 00:00:00

pages

47-58

issue

1

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(14)00780-0

journal_volume

358

pub_type

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