Traditional Chinese medicine for prevention and treatment of hepatocarcinoma: From bench to bedside

Hu, Bing; Wang, Shuangshuang; Du, Qin

doi:10.4254/wjh.v7.i9.1209

Cited by 61 publications

(42 citation statements)

References 116 publications

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“…It has previously been reported that the Dox-induced apoptotic mechanism is reactive oxygen species-dependent in normal cells and p53-dependent in cancer cells (39). In addition, SPPC, the extract of L. japonica, was shown to promote apoptosis by downregulating IL-10 expression (40). The present study demonstrated that SPPC reduced the viability of breast cancer cells and that, when used in combination with DOX, it was able to promote the apoptosis of breast cancer cells, while simultaneously reducing the dose and adverse effects of Dox.…”

Section: A B C Dmentioning

confidence: 99%

Sulfated polysaccharide-protein complex sensitizes doxorubicin-induced apoptosis of breast cancer cells in vitro and in vivo

Wang

Zhou

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to investigate the effect of sulfated polysaccharide-protein complex (SPPC) on the antitumor effect of doxorubicin (Dox) on MDA-MB-231 breast cancer cells in vitro and in vivo. MTT and Annexin V/propidium iodide staining assays demonstrated that SPPC selectively sensitized MDA-MB-231 cells to Dox-induced cytotoxicity. The half maximal inhibitory concentration of Dox against MDA-MB-231 cells was decreased from 5.3 to 1.5 µM when it was used concomitantly with 5 µM SPPC. SPPC potentiated Dox-induced apoptosis in breast cancer cells via the mitochondrial apoptosis signaling pathway by activating caspase-3 and caspase-9. Notably, the caspase inhibitor Z-VAD-fmk diminished the effect of SPPC on Dox-mediated apoptosis. Furthermore, combination treatment with SPPC and Dox markedly reduced the growth of breast cancer xenografts in mice. The present study demonstrated that SPPC was able to enhance the antitumor effect of Dox on breast cancer cells, thus suggesting that SPCC may be used to reduce the cumulative dose of Dox and its associated toxicities in the chemotherapy of breast cancer and other types of cancer.

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Section: A B C Dmentioning

confidence: 99%

Sulfated polysaccharide-protein complex sensitizes doxorubicin-induced apoptosis of breast cancer cells in vitro and in vivo

Wang

Zhou

et al. 2016

Experimental and Therapeutic Medicine

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“…In order to guarantee the validity and reliability, evidence-based preclinical and clinical explorations are required. Moreover, elucidation of the underlying pharmaceutical mechanism could bene t the acceptance of TCM application [12][13][14][33][34][35].…”

Section: Gjf Inhibited the Activation Of Mitosis-related Protein Of Hmentioning

confidence: 99%

“…Recent studies have indicated that TCM can induce cell-cycle arrest and attenuate the tumor-associated macrophage-stimulated proliferation to inhibit tumor proliferation [12][13][14]. In addition, more and more researches con rmed the synergism and detoxi cation of combination of TCM with chemo-or radiotherapy [15].…”

Section: Introductionmentioning

confidence: 99%

Chinese Formula Ganji Fang Inhibits Tumor Growth Through Regulating Cell Mitosis by Reducing ARPP-19 Expression in Hepatocellular Carcinoma

Zhang¹,

Tang²,

Yang³

et al. 2020

Preprint

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Background: Hepatocellular carcinoma (HCC) is one of the most common malignancies with high rate of mortality worldwide. Rare effective treatment is available for HCC patients especially at advanced stage. Ganji Fang (GJF), one formula of traditional Chinese medicine (TCM), has shown therapeutic effect on HCC in clinical application. This study aims at evaluating the anti-HCC effect and safety of GJF treatment, as well as exploring the potential underlying molecular mechanism by using HCC mouse model. Methods: HepG2 cells were subcutaneously injected into the upper flank of male BALB/c nude mice to establish the HCC Xenograft model. Mice were randomly assigned to three groups, treated respectively with high (GJF-H group) or low dose (GJF-L group) of GJF or vehicle (Control group) via gavage. The tumor volume was detected dynamically. Four weeks later, the weight and proliferation activity of tumors were measured. Western blot and immunohistochemistry were used to detect the expression of cAMP-regulated phosphoprotein 19 (ARPP-19) and the regulated molecules. H&E staining of tissue section of liver and kidney was used to assess the toxicity of the formula. Foe investigation of survival time, SMMC 7721 cells were injected subcutaneously to the BALB/c-nude mice. The tumor-bearing mice were allocated into two groups (Control and GJF-H) and treated as above description. The death number of mice was recorded and the survival time was analyzed.Results: Compared with control, the body weight and activity of GJF-treated mice were improved obviously. No toxic change was observed in tissues of liver and kidney. The tumor volume and weight was significantly down-regulated by GJF dose-dependently. The mice with GJF treatment showed the tendency of prolonging survival time. The proliferation index and PCNA expression in the tumor of GJF group were lower than in control. Furthermore, GJF down-regulated levels of ARPP-19 and phospho-(Ser) CDKs substrates, up-regulated level of inactivated cyclin division cycle 2 (Cdc2). Conclusion: GJF can effectively inhibit tumor growth of HCC and improve the general condition of the nude mouse xenograft model. The mechanism of inhibiting tumor growth is partially related to down-regulating ARPP-19 to inhibit mitosis and cell proliferation of HCC.

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“…During this period, the treatment options for HCC have expanded to include additional chemotherapeutic agents and targeted therapies (21,22). In recent years, traditional Chinese medicine (TCM), or its extractions, have had a positive role in the treatment of cancer (23,24).…”

Section: Introductionmentioning

confidence: 99%

Role of S100A3 in human hepatocellular carcinoma and the anticancer effect of sodium cantharidinate

Tao

Wang

Qiu

et al. 2017

Experimental and Therapeutic Medicine

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The fifth most common cancer worldwide is hepatocellular carcinoma (HCC), which has an annual mortality rate of ~800,000. Although surgical procedures for HCC, such as hepatic resection and liver transplantation, have progressed and the outcomes of patients have improved, HCC is still characterized by frequent recurrence, even after liver transplantation. In the present study the expression of the protein coding gene, S100 calcium binding protein A3 (S100A3), was observed in 62 HCC tissues and tumor-surrounding tissues. The present study indicated that S100A3 activation was involved in tumorigenesis and tumor aggressiveness. The protein and mRNA expression levels of S100A3 in the human HCC cell line (HepG2) were investigated using western blotting and reverse transcription-quantitative polymerase chain reaction analysis, respectively. The function of sodium cantharidinate in inducing HCC cell apoptosis was also investigated. Sodium cantharidinate inhibited the protein and gene expression of S100A3 in HepG2 cells in vitro. These data suggested that S100A3 has an important role in human HCC. The present study indicates that the functional properties of sodium cantharidinate are promising for the development of a novel drug that may control the expression of S100A3 and improve the treatment of human HCC in the near future.

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Traditional Chinese medicine for prevention and treatment of hepatocarcinoma: From bench to bedside

Cited by 61 publications

References 116 publications

Sulfated polysaccharide-protein complex sensitizes doxorubicin-induced apoptosis of breast cancer cells in vitro and in vivo

Sulfated polysaccharide-protein complex sensitizes doxorubicin-induced apoptosis of breast cancer cells in vitro and in vivo

Chinese Formula Ganji Fang Inhibits Tumor Growth Through Regulating Cell Mitosis by Reducing ARPP-19 Expression in Hepatocellular Carcinoma

Role of S100A3 in human hepatocellular carcinoma and the anticancer effect of sodium cantharidinate

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