Oligonol, a Low Molecular Weight Polyphenol, Enhances Apoptotic Cell Death in Ovarian Cancer Cells via Suppressing NF-κB Activation

Kim, Miseon; Park, Wook Ha; Lee, Seul; Suh, Dong Hoon; Kim, Kidong; No, Jae Hong; Kim, Yong Beom

doi:10.1080/01635581.2018.1557215

Cited by 5 publications

(3 citation statements)

References 31 publications

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“…It indicated that lipid metabolism might be disordered in ovarian cancer. 6 Oxidative Medicine and Cellular Longevity…”

Section: Kegg Pathway Analysis Revealed Lipid Metabolismmentioning

confidence: 99%

“…Cancer cells showed greater ROS stress compared to normal cells, partly due to increased metabolic activity, carcinogenesis stimulation, and mitochondrial malfunction [ 5 ]. In ovarian cancer, the previous studies showed that ROS could activate various oncogenic transcription factors such as NF- κ B [ 6 ], AP-1 [ 7 ], and STAT3 [ 8 ], to influence cellular transformation, tumor cell proliferation, inflammation, tumor cell survival, metastasis and invasion, and angiogenesis. Moreover, molecular and cellular function analysis of ovarian cancer mitochondrial expressed proteins (mtEPs) found that many mitochondrial differentially expressed proteins (mtDEPs) were associated with ROS production, such as generation of active oxygen species, metabolism of hydrogen peroxide, and synthesis, metabolism, production, and quantity of ROS [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

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HSP60 Regulates Lipid Metabolism in Human Ovarian Cancer

Wen

et al. 2021

Oxidative Medicine and Cellular Longevity

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Accumulating evidence demonstrates that cancer is an oxidative stress-related disease, and oxidative stress is closely linked with heat shock proteins (HSPs). Lipid oxidative stress is derived from lipid metabolism dysregulation that is closely associated with the development and progression of malignancies. This study sought to investigate regulatory roles of HSPs in fatty acid metabolism abnormality in ovarian cancer. Pathway network analysis of 5115 mitochondrial expressed proteins in ovarian cancer revealed various lipid metabolism pathway alterations, including fatty acid degradation, fatty acid metabolism, butanoate metabolism, and propanoate metabolism. HSP60 regulated the expressions of lipid metabolism proteins in these lipid metabolism pathways, including ADH5, ECHS1, EHHADH, HIBCH, SREBP1, ACC1, and ALDH2. Further, interfering HSP60 expression inhibited migration, proliferation, and cell cycle and induced apoptosis of ovarian cancer cells in vitro. In addition, mitochondrial phosphoproteomics and immunoprecipitation-western blot experiments identified and confirmed that phosphorylation occurred at residue Ser70 in protein HSP60, which might regulate protein folding of ALDH2 and ACADS in ovarian cancers. These findings clearly demonstrated that lipid metabolism abnormality occurred in oxidative stress-related ovarian cancer and that HSP60 and its phosphorylation might regulate this lipid metabolism abnormality in ovarian cancer. It opens a novel vision in the lipid metabolism reprogramming in human ovarian cancer.

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“…It indicated that lipid metabolism might be disordered in ovarian cancer. 6 Oxidative Medicine and Cellular Longevity…”

Section: Kegg Pathway Analysis Revealed Lipid Metabolismmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

HSP60 Regulates Lipid Metabolism in Human Ovarian Cancer

Wen

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Oligonol is a phenolic phytochemical consisting of catechin monomers, procyanidin dimers, and oligomers of proanthocyanidins [ 17 ]. Oligonol has exhibited strong anti-oxidant and anti-inflammation activities, serving as a promising candidate for the treatment of cancer as well as inflammatory and metabolic disorders [ 18 , 19 ]. Furthermore, oligonol possesses anti-aging properties that can prevent photoaging by mitigating changes that would cause dysregulation of wound healing, collagen synthesis, and growth factor production [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Integrative Transcriptomic Analysis Reveals Upregulated Apoptotic Signaling in Wound-Healing Pathway in Rat Liver Fibrosis Models

Kim,

Lee,

Noh

et al. 2023

Antioxidants

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Liver fibrosis, defined by the aberrant accumulation of extracellular matrix proteins in liver tissue due to chronic inflammation, represents a pressing global health issue. In this study, we investigated the transcriptomic signatures of three independent liver fibrosis models induced by bile duct ligation, carbon tetrachloride, and dimethylnitrosamine (DMN) to unravel the pathological mechanisms underlying hepatic fibrosis. We observed significant changes in gene expression linked to key characteristics of liver fibrosis, with a distinctive correlation to the burn-wound-healing pathway. Building on these transcriptomic insights, we further probed the p53 signaling pathways within the DMN-induced rat liver fibrosis model, utilizing western blot analysis. We observed a pronounced elevation in p53 protein levels and heightened ratios of BAX/BCL2, cleaved/pro-CASPASE-3, and cleaved/full length-PARP in the livers of DMN-exposed rats. Furthermore, we discovered that orally administering oligonol—a polyphenol, derived from lychee, with anti-oxidative properties—effectively countered the overexpressions of pivotal apoptotic genes within these fibrotic models. In conclusion, our findings offer an in-depth understanding of the molecular alterations contributing to liver fibrosis, spotlighting the essential role of the apoptosis pathway tied to the burn-wound-healing process. Most importantly, our research proposes that regulating this pathway, specifically the balance of apoptosis, could serve as a potential therapeutic approach for treating liver fibrosis.

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