We are analyzing https://link.springer.com/article/10.1007/s00109-012-0966-0.

Title:
Inhibition of autophagy enhances anticancer effects of bevacizumab in hepatocarcinoma | Journal of Molecular Medicine
Description:
Angiogenesis inhibitors have long been considered desirable anticancer agents. However, it was found that many tumors could develop resistance to antiangiogenesis inhibitors. Antiangiogenic therapy results in metabolic stress. Autophagy is an important survival mechanism in cancer cells under metabolic stress; however, it remains unknown if autophagy contributes to antiangiogenesis resistance. In this study, we reported that bevacizumab treatment reduced the development of new blood vessels and inhibited cell growth in xenografts of hepatocellular carcinoma (HCC) tumors. Bevacizumab treatment also upregulated expression of the autophagy-related genes (Beclin1 and LC3) and increased autophagosome formation. Our in vitro studies demonstrated that autophagy inhibition significantly increased apoptosis of HCC cells during nutrient starvation or hypoxia. In addition, the combined treatment of an autophagy inhibitor and bevacizumab markedly inhibited the tumor growth of HCC xenografts, led to enhanced apoptosis, and impaired the proliferation of tumor cells compared with treatment with either drug alone. Furthermore, autophagy inhibition led to enhanced reactive oxygen species (ROS) generation in HCC cells exposed to nutrient starvation or hypoxia in vitro and increased DNA oxidative damage in vivo. Antioxidants reduced nutrient starvation or the hypoxia-induced cell death of HCC cells after autophagy inhibition. Our results suggest that autophagy modulates ROS generation and contributes to cell survival under metabolic stress. Therefore, autophagy inhibition may be a novel way of increasing the efficicacy of antiangiogenic agents in the treatment of HCC.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

autophagy, cells, tumor, cell, bevacizumab, treatment, article, hcc, fig, google, scholar, pubmed, ros, cas, apoptosis, nutrient, inhibition, hypoxia, xenograft, shown, tumors, stress, analysis, smmc, results, group, data, metabolic, staining, bar, antiangiogenic, cancer, growth, increased, starvation, death, apoptotic, hepb, combination, scale, hepatocarcinoma, survival, reduced, beclin, generation, medium, full, antiangiogenesis, significantly, compared,

Topics {✒️}

gfp-lc3 punctate dots/cell bcr-abl-mediated leukemogenesis article download pdf cm-h2dcfda/dcfh-da environmentally-induced oxidative stress mouse anti-hif-1α streptavidin–biotin complex method li-xin wei rabbit anti-activated caspase-3 unique autophagy-related protein multiple-center intratumoral injections reduced microvessel density beta-catenin levels gfp-tagged lc3 plasmid cq-treated nutrient-starved cells humanized monoclonal antibody dna oxidative damage nutrient-deficient hcc cells nutrient-starved smmc7721 cells activated caspase-3-positive cells western blot analysis nutrient-starved hcc cells hypoxia-induced cell death sirna-mediated inhibition rabbit anti-cd31 privacy choices/manage cookies resist antiangiogentic therapy hepatocarcinoma xenograft model rabbit anti-lc3 reactive oxygen species anti-osteoclastogenic action gfp-lc3 dots rabbit anti-pcna htert enhances chemosensitivity rabbit anti-beclin1 article guo dcf-da staining related subjects increased intratumoral apoptosis open access gfp-lc3 plasmid gfp-tagged lc3 hypoxia-induced autophagy contributes jian-rui song xenograft tumor tissue woodchuck hepatoma model gene therapy center significantly increased number nutrient-deficient condition desirable anticancer agents

Questions {❓}

Moon WS, Rhyu KH, Kang MJ, Lee DG, Yu HC, Yeum JH, Koh GY, Tarnawski AS (2003) Overexpression of VEGF and angiopoietin 2: a key to high vascularity of hepatocellular carcinoma?

Schema {🗺️}

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      headline:Inhibition of autophagy enhances anticancer effects of bevacizumab in hepatocarcinoma
      description:Angiogenesis inhibitors have long been considered desirable anticancer agents. However, it was found that many tumors could develop resistance to antiangiogenesis inhibitors. Antiangiogenic therapy results in metabolic stress. Autophagy is an important survival mechanism in cancer cells under metabolic stress; however, it remains unknown if autophagy contributes to antiangiogenesis resistance. In this study, we reported that bevacizumab treatment reduced the development of new blood vessels and inhibited cell growth in xenografts of hepatocellular carcinoma (HCC) tumors. Bevacizumab treatment also upregulated expression of the autophagy-related genes (Beclin1 and LC3) and increased autophagosome formation. Our in vitro studies demonstrated that autophagy inhibition significantly increased apoptosis of HCC cells during nutrient starvation or hypoxia. In addition, the combined treatment of an autophagy inhibitor and bevacizumab markedly inhibited the tumor growth of HCC xenografts, led to enhanced apoptosis, and impaired the proliferation of tumor cells compared with treatment with either drug alone. Furthermore, autophagy inhibition led to enhanced reactive oxygen species (ROS) generation in HCC cells exposed to nutrient starvation or hypoxia in vitro and increased DNA oxidative damage in vivo. Antioxidants reduced nutrient starvation or the hypoxia-induced cell death of HCC cells after autophagy inhibition. Our results suggest that autophagy modulates ROS generation and contributes to cell survival under metabolic stress. Therefore, autophagy inhibition may be a novel way of increasing the efficicacy of antiangiogenic agents in the treatment of HCC.
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      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Hang Zhou Sanitarium of Navy, Zhejiang, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Department of Oncology, Chang Zheng Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China
      name:Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, People’s Republic of China

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