miR-324-5p could suppress mitochondrial fragmentation, promote membrane potential, and ATP levels, as well as protect against oxidative stress-induced EPCs apoptosis. Our results suggested that miR-324-5p protects against oxidative stress-induced EPCs injury by regulating Mtfr1....
SOCS2-AS1 depletion repressed the proliferation of HUVECs, whereas it facilitated apoptosis. Further, SOCS2-AS1 could bind with miR-324-5p and negatively regulated miR-324-5p expression in HUVECs. Besides, CUE domain containing 2 (CUEDC2) was the downstream target of miR-324-5p, and SOCS2...
miR-324-5p KLF3 proliferation apoptosis pancreatic cancer Introduction Pancreatic cancer, as one of the most aggressive malignancies with the mortality rate as high as 80% and the 5-year survival rate as low as 8%, is the second leading cause of death in digestive system malignant diseases in...
3b). The cell apoptosis results showed that the overexpression of miR-324-5p inhibited cell apoptosis rate, while the inhibition of miR-324-5p led to enhanced cell apoptosis rate in both AGS and MKN45 cell lines (all P < 0.01, Fig. 3c). Transwell assays were performed to assess the ...
39 miR-324-5p has also been reported to promote apoptosis and oxidative stress by targeting Mtfr1,29 indicating that miR-324-5p is tightly associated with mitochondrial function. As lipid deposition requires mitochondrial-provided ATP,40 we hypothesize that miR-324-5p promotes oleate-induced lipid ...
Moreover, miR-324-5p inhibited the viability and induced the apoptosis of gastric cancer cells in vitro. TSPAN8 is a functional target of miR-324-5p in gastric cancer. MiR-324-5p was further confirmed to reduce gastric cancer cell viability and induce apoptosis via downregulating TSPAN8 in ...
Mtfr1 is a direct target of miR-324-5p, and miR-324-5p attenuates mitochondrial fission, cardiomyocyte apoptosis and myocardial infarction by suppressing Mtfr1 translation. Finally, we show that transcription factor NFAT4 inhibits miR-324-5p expression. Knockdown of NFAT4 suppresses mitochondrial ...
Mtfr1 is a direct target of miR-324-5p, and miR-324-5p attenuates mitochondrial fission, cardiomyocyte apoptosis and myocardial infarction by suppressing Mtfr1 translation. Finally, we show that transcription factor NFAT4 inhibits miR-324-5p expression. Knockdown of NFAT4 suppresses mitochondrial ...
CircATIC interference notably hampered cell proliferation, migration, invasion, and glycolysis and induced cell apoptosis of MM cells. MiR-324-5p was a target of circATIC. CircATIC silencing-mediated effects in MM cells were largely overturned by the knockdown of miR-324-5p. HGF was a target...
Our study defines the NFAT4/ miR-324-5p/Mtfr1 axis, which participates in the regulation of mitochondrial fission and cardiomyocyte apoptosis, and suggests potential new treatment avenues for cardiac diseases. 展开 DOI: 10.1038/cddis.2015.348 被引量: 8 ...