Novel Investigations of Flavonoids as Chemopreventive Agents for Hepatocellular Carcinoma

Liao, Chenyi; Lee, Ching-Chang; Tsai, Chia-Wen; Hsueh, Chao-Wen; Wang, Chih-Chiang; Chen, I-Hung; Tsai, Ming-Kai; Liu, Meiyu; Hsieh, An-Tie; Su, Kuan-Jen; Wu, Hau-Ming; Huang, Shih-Chung; Wang, Yi-Chen; Wang, Chien-Yao; Huang, Steve S.; Yeh, Yen-Cheng; Ben, Ren-Jy; Chien, Shang‐Tao; Hsu, Chin‐Wen; Kuo, Wu‐Hsien

doi:10.1155/2015/840542

Cited by 64 publications

(37 citation statements)

References 240 publications

(279 reference statements)

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“…Cytokines, chemokines, pH value, hypoxia, fibroblast and extracellular matrix proteins are important components of the tumor microenvironment[18-21]. The tumor microenvironment plays an important role in regulating tumor progression[22,23]. It has been reported that many extracellular matrix proteins exert significant influence on tumor progression.…”

Section: Discussionmentioning

confidence: 99%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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AIMTo determine the influence of Smoc2 on hepatocellular carcinoma (HCC) cell proliferation and to find a possible new therapeutic target for preventing HCC progression.METHODSWe detected expression of Smoc2 in HCC tissues and corresponding non-tumor liver (CNL) tissues using PCR, western blot, and immunohistochemistry methods. Subsequently, we down-regulated and up-regulated Smoc2 expression using siRNA and lentivirus transfection assay, respectively. Then, we identified the effect of Smoc2 on cell proliferation and cell cycle using CCK-8 and flow cytometry, respectively. The common cell growth signaling influenced by Smoc2 was detected by western blot assay.RESULTSThe expression of Smoc2 was significantly higher in HCC tissues compared with CNL tissues. Overexpression of Smoc2 promoted HCC cell proliferation and cell cycle progression. Down-regulation of Smoc2 led to inhibition of cell proliferation and cell cycle progression. Smoc2 had positive effect on ERK and AKT signaling.CONCLUSIONSmoc2 promotes the proliferation of HCC cells through accelerating cell cycle progression and might act as an anti-cancer therapeutic target in the future.

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Section: Discussionmentioning

confidence: 99%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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“…Flavonoids are safe and reliable agents that are extracted from natural products, which show a broad spectrum of biological activities with fewer side effects[116]. Phloretin is a natural phenol which could be extracted from manchurian apricot and apple tree leaves.…”

Section: Regulatory Mechanism Of Glucose Metabolic Reprogrammingmentioning

confidence: 99%

Reprogramming of glucose metabolism in hepatocellular carcinoma: Progress and prospects

Shang

Wang

2016

WJG

108

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Hepatocellular carcinoma (HCC) is one of the most lethal cancers, and its rate of incidence is rising annually. Despite the progress in diagnosis and treatment, the overall prognoses of HCC patients remain dismal due to the difficulties in early diagnosis and the high level of tumor invasion, metastasis and recurrence. It is urgent to explore the underlying mechanism of HCC carcinogenesis and progression to find out the specific biomarkers for HCC early diagnosis and the promising target for HCC chemotherapy. Recently, the reprogramming of cancer metabolism has been identified as a hallmark of cancer. The shift from the oxidative phosphorylation metabolic pathway to the glycolysis pathway in HCC meets the demands of rapid cell proliferation and offers a favorable microenvironment for tumor progression. Such metabolic reprogramming could be considered as a critical link between the different HCC genotypes and phenotypes. The regulation of metabolic reprogramming in cancer is complex and may occur via genetic mutations and epigenetic modulations including oncogenes, tumor suppressor genes, signaling pathways, noncoding RNAs, and glycolytic enzymes etc. Understanding the regulatory mechanisms of glycolysis in HCC may enrich our knowledge of hepatocellular carcinogenesis and provide important foundations in the search for novel diagnostic biomarkers and promising therapeutic targets for HCC.

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“…to suppress HCC proliferation, survival, and metastasis through induction of apoptosis and inhibition of signaling transduction which participates in tumor progression (7)(8)(9). In addition, some studies reported herbal medicine combined with chemotherapy to improve survival and tumor response compared to chemotherapy alone in the treatment of patients with HCC (10).…”

mentioning

confidence: 99%

Magnolol Induces Apoptosis and Inhibits ERK-modulated Metastatic Potential in Hepatocellular Carcinoma Cells

Kuan

Chen

et al. 2018

In Vivo

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Background/Aim: The aim of the present study was to evaluate the anti-cancer effect of magnolol in hepatocellular carcinoma (HCC) cells in vitro. Materials and Methods: HCC SK-Hep1 cells were treated with different concentrations of magnolol or PD98059 [extracellular-signal-regulated kinase (ERK) inhibitor] for 48 h, and then cell viability, apoptosis, signal transduction, expression of anti-apoptotic and metastasis-related proteins, and cell invasion were investigated by [3][4]-2,5-diphenyltetrazolium bromide] (MTT) assay, flow cytometry, nuclear factor kappa B (NF-ĸB) reporter gene, western blotting, and cell invasion assays. Results: Magnolol significantly induced accumulation of sub-G 1 phase and caspase-3 activation and inhibited NF-ĸB activation, cell invasion, expression of phosphorylated ERK (pERK), anti-apoptotic and metastatic-related proteins. ERK inactivation was required for magnolol-induced inhibition of metastatic potential of SK-Hep1 cells. Conclusion: Taken together, these results indicated that magnolol not only induced apoptosis, but also inhibited ERK-modulated metastatic potential of HCC SK-Hep1 cells.

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Novel Investigations of Flavonoids as Chemopreventive Agents for Hepatocellular Carcinoma

Cited by 64 publications

References 240 publications

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Reprogramming of glucose metabolism in hepatocellular carcinoma: Progress and prospects

Magnolol Induces Apoptosis and Inhibits ERK-modulated Metastatic Potential in Hepatocellular Carcinoma Cells

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