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Mitochondrial dysfunction suppresses p53 expression via calcium-mediated nuclear factor-kB signaling pathway in HCT116 human colorectal-carcinoma cells.
Yung-Jin Kim1,*, Eui-Yeun Yi1,#, Young-Kyoung Lee1,#, Shi-Young Park Park1, Won-Jun Jang1, Yu-Seon Han1, Myeong-Eun Jegal1
1Molecular Biology, Pusan National University
Abstract
Mitochondrial DNA (mtDNA) mutations are often observed in various cancer types. Although correlation between mitochondrial dysfunction and cancer malignancy have been demonstrated by several researchers, more research is required to elucidate the molecular mechanisms underlying accelerated tumor development and progression due to mitochondrial mutations. We generated an mtDNA-depleted cell line, ヱ0, through long-term ethidium bromide treatment to define the molecular mechanism of tumor malignancy induced by mitochondrial dysfunction. Mitochondrial dysfunction in ヱ0 cells reduced drug-induced cell death and decreased expression of pro-apoptotic protein including p53. p53 expression was reduced on activation of the nuclear factor-リB that depended on elevated levels of free calcium in HCT116/ヱ0 cells. Taken together, these data provide a novel mechanism for tumor development and drug resistance due to mitochondrial dysfunction.
Abstract, Accepted Manuscript(in press) [Submitted on December 7, 2017, Accepted on March 5, 2018]
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