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Hangzhou, China

Zhao P.,Health Management Center | Mao J.-M.,Hangzhou Sanatorium of PLA | Zhou Z.-Q.,Health Management Center | Tan Y.,Health Management Center | Zhang Y.,Health Management Center
Oncology Letters

Quercetin can inhibit the growth of cancer cells with the ability to act as a 'chemopreventer'. Its cancer-preventive effect has been attributed to various mechanisms, including the induction of cell-cycle arrest and/or apoptosis, as well as its antioxidant functions. Quercetin can also reduce adipogenesis. Previous studies have shown that quercetin has potent inhibitory effects on animal fatty acid synthase (FASN). In the present study, activity of quercetin was evaluated in human liver cancer HepG2 cells. Intracellular FASN activity was calculated by measuring the absorption of NADPH via a spectrophotometer. MTT assay was used to test the cell viability, immunoblot analysis was performed to detect FASN expression levels and the apoptotic effect was detected by Hoechst 33258 staining. In the present study, it was found that quercetin could induce apoptosis in human liver cancer HepG2 cells with overexpression of FASN. This apoptosis was accompanied by the reduction of intracellular FASN activity and could be rescued by 25 or 50 μM exogenous palmitic acids, the final product of FASN-catalyzed synthesis. These results suggested that the apoptosis induced by quercetin was via the inhibition of FASN. These findings suggested that quercetin may be useful for preventing human liver cancer. Source

Lin L.L.,Wuxi Higher Health Vocational Technology School | Wang W.,Hangzhou Sanatorium of PLA | Hu Z.Y.,Cancer Research Institute | Wang L.W.,Wuxi Higher Health Vocational Technology School | And 2 more authors.
Medical Oncology

Primary hepatocellular carcinoma (HCC) is the most common form of liver cancer and is one of the most common malignancies worldwide. Tumor suppressor gene silencing through DNA methylation contributes to cancer formation. The ten–eleven translocations (TET) family of α-ketogluta-rate-dependent dioxygenases catalyzes the sequential oxidation of 5-methylcytosine to 5-hydroxymethyl-cytosine, 5-formylcytosine and 5-carboxylcytosine, leading to eventual DNA demethylation. MicroRNAs are an abundant class of 17–25 nucleotides small noncoding RNAs, identified as important regulators of many diverse biological processes. In this study, we showed that TET1 expression was obviously reduced in the majority of examined HCC tissues. And we further investigated the expression and functional involvement of TET1 in proliferation, migration and invasion, and determined that TET1 may function as a tumor suppressor. MiR-29b was proved to inhibit metastasis through the targeting of TET1, indicating that downregulation of miR-29 may involve in HCC carcinogenesis and progression through potentiation of TET1 expression. Thus, we elucidated the roles of feedback of miR-29-TET1 downregulation in HCC development and suggested a potential target in identification of the prognosis and application of cancer therapy for HCC patients. © 2014, Springer Science+Business Media New York. Source

Hu Z.,Hangzhou Cancer Institute | Wang W.,Hangzhou Sanatorium of PLA | Ling J.,Hangzhou Sanatorium of PLA | Jiang C.,Hangzhou First Peoples Hospital
Cellular and Molecular Neurobiology

Microglia-mediated neuroinflammation induced by α-synuclein in the substantianigra likely either initiates or aggravates nigral neuro degeneration in Parkinson’s disease (PD). We aimed to explore the effects of α-mangostin (α-M), a polyphenolicxanthone derivative from mangosteen on α-synuclein-stimulated DA neurodegeneration. Primary microglia, mesencephalic neuron, mesencephalic neuron-glianeuronal cultures, and transwell co-cultures were prepared separately. Liquid scintillation counting was used to determine the radioactivity in DA uptake. Enzyme-linked immunosorbent assay (ELISA) was performed in the IL-1β, IL-6, and TNF-α assay. The expression of proteins was analyzed by Western blot. α-M inhibited the increased levels of pro-inflammatory cytokines, NO, and ROS in α-synuclein-stimulated primary microglia. Mechanistic study revealed that α-M functioned by inhibition of nuclear factor kappa B (NF-κB) and NADPH oxidase. Further, α-M protected α-synuclein-induced microglial and direct neurotoxicity. Although detailed mechanisms remain to be defined, our observations suggest a potential compound, which inhibits microglial activation induced by α-synuclein by targeting NADPH oxidase, might be a therapeutic possibility in preventing PD progression. © 2016 The Author(s) Source

Luo Y.,Hangzhou Sanatorium of PLA | Wang S.-X.,Hangzhou Sanatorium of PLA | Zhou Z.-Q.,Hangzhou Sanatorium of PLA | Wang Z.,Hangzhou Sanatorium of PLA | And 3 more authors.
Tumor Biology

Genistein possesses a wide variety of biological activities, and it is best known for its ability to inhibit cancer progression. Its cancer-preventive effect has been attributed to various mechanisms, including the induction of cell cycle arrest and apoptosis as well as the antioxidant functions. Nuclear factor kappa-B (NF-κB) is a signaling pathway that controls transcriptional activation of genes important for the tight regulation of many cellular processes and is aberrantly expressed in many types of cancer. Inhibitors of NF-κB pathway have shown potential anti-tumor activities. However, it is not fully elucidated in colon cancer. In the present study, we demonstrated that genistein could induce apoptosis in human colon cancer LoVo and HT-29 cells through inhibiting NF-κB pathway, as well as downregulation of Bcl-2 and upregulation of Bax, thus providing basis for clinical application of genistein in colon cancer cases. © 2014, International Society of Oncology and BioMarkers (ISOBM). Source

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