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• W2038162169 startingPage "10159" @default.
• W2038162169 abstract "Verrucarin A (VA), an active constituent of pathogenic fungus Myrothecium verrucaria, which has the ability to inhibit the growth of breast cancer cells. However, the mechanism by which VA exerts its inhibitory potential remains elusive. Here, we demonstrated that VA inhibited the growth of MCF-7 breast cancer cells, increased the levels of reactive oxygen species (ROS), and subsequently induced mitochondrial membrane potential (Δψm) loss, leading to the increase of Bax/Bcl-2 ratio, cytochrome c release, caspase activation, PARP degradation, and apoptosis. VA effectively increased the phosphorylation of p38MAPK and diminished the phosphorylation of ERK/Akt. In addition, VA caused cell cycle deregulation through the induction of p21 and p53. Furthermore, ROS scavenger (n-acetyl-l-cysteine) and p38MAPK inhibitor (SB202190) effectively abrogated the VA-induced cell cycle deregulation and apoptosis. Conversely, U0126, an ERK1/2 inhibitor, enhanced the VA-induced apoptotic signals. Taken together, our results suggest that VA-induces apoptosis and cell cycle deregulation in MCF-7 cells through ROS-dependent p38MAPK activation." @default.
• W2038162169 created "2016-06-24" @default.
• W2038162169 creator A5029168779 @default.
• W2038162169 creator A5067816527 @default.
• W2038162169 creator A5068268402 @default.
• W2038162169 date "2014-07-16" @default.
• W2038162169 modified "2023-10-18" @default.
• W2038162169 title "Verrucarin A alters cell-cycle regulatory proteins and induces apoptosis through reactive oxygen species-dependent p38MAPK activation in the human breast cancer cell line MCF-7" @default.
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• W2038162169 doi "https://doi.org/10.1007/s13277-014-2286-1" @default.
• W2038162169 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25027398" @default.
• W2038162169 hasPublicationYear "2014" @default.
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