2019
DOI: 10.7841/ksbbj.2019.34.3.185
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Apoptotic Effects of Parthenocissus tricuspidata (Siebold & Zucc.) Planch Ethanol Extract by regulating AMPK/Akt/mTOR Signaling Pathways in A549 Cancer Cells

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Cited by 2 publications
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“…In intracellular mitochondria, AMPK-ɑ promotes a catabolism mode, contributes to the establishment of the glutamine degradation pathway, or induces phosphorylation of the tumor suppressor protein p53 at Ser15 and accumulation in the mitochondria (Liang & Mills, 2013;Park et al, 2003). When phosphorylated p53 on the mitochondrial surface increases, the complex which is formed by Bcl-2, which promotes cell viability in the endogenous pathway, and Bax, a protein that liberates cytochrome c from mitochondria and induces apoptosis, is rearranged and apoptosis occurs through their antagonism (Jo et al, 2019). Therefore, the anticancer mechanism through apoptosis is the accumulation of phosphorylated p53 by the increase of AMPK in cancer cell, reducing Bcl-2 that inhibits apoptosis and increasing Bax that promotes apoptosis, resulting in loss of cell membrane potential and induces apoptosis through the destruction of the mitochondrial membrane and release of cytochrome c (Park et al, 2018;Cho et al, 2016).…”
Section: Assessment Of Inhibition Of Breast Cancer Cell Proliferationmentioning
confidence: 99%
“…In intracellular mitochondria, AMPK-ɑ promotes a catabolism mode, contributes to the establishment of the glutamine degradation pathway, or induces phosphorylation of the tumor suppressor protein p53 at Ser15 and accumulation in the mitochondria (Liang & Mills, 2013;Park et al, 2003). When phosphorylated p53 on the mitochondrial surface increases, the complex which is formed by Bcl-2, which promotes cell viability in the endogenous pathway, and Bax, a protein that liberates cytochrome c from mitochondria and induces apoptosis, is rearranged and apoptosis occurs through their antagonism (Jo et al, 2019). Therefore, the anticancer mechanism through apoptosis is the accumulation of phosphorylated p53 by the increase of AMPK in cancer cell, reducing Bcl-2 that inhibits apoptosis and increasing Bax that promotes apoptosis, resulting in loss of cell membrane potential and induces apoptosis through the destruction of the mitochondrial membrane and release of cytochrome c (Park et al, 2018;Cho et al, 2016).…”
Section: Assessment Of Inhibition Of Breast Cancer Cell Proliferationmentioning
confidence: 99%