Summary: | 碩士 === 國立臺灣大學 === 生化科技學系 === 101 === Except for providing ATP, mitochondria also regulate cell growth, death, and differentiation. Many studies showed that mitochondrial dysfunction involved in many diseases, like neurodegenerative disease, myopathy, and cancer. It has been shown that mitochondrial dysfunction might affect the expression profile of nuclear genes via the so called “mitochondrial retrograde signaling”. Previously, our lab found that the migration and invasion ability of the PDT-derived variants was significantly decreased. Meanwhile, a small molecule named “BMVC-12C” has been found to localize in mitochondria. In this study, we would like to examine whether BMVC-12C can induce mitochondrial dysfunction and further investigate the following biological consequences. We found out that BMVC-12C can inhibit cell growth at low concentration. Further studies showed that BMVC-12C treatment led to mitochondrial dysfunction and the production of reactive oxygen species (ROS) was also observed. Meanwhile, we found that the BMVC-12C could inhibit the replication of mitochondrial DNA (mtDNA). Finally, we showed that BMVC-12C treatment can reduce cell migration ability and the expression level of PEG-1/MEST gene
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