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Keywords {🔍}

cells, hifα, hcc, pubmed, article, snai, emt, expression, google, scholar, metastasis, hypoxia, cancer, cas, cell, figure, invasion, ecadherin, data, ncadherin, tumor, vimentin, smmc, file, additional, carcinoma, shown, hre, central, factor, prognosis, migration, level, transition, table, performed, luciferase, samples, analysis, hypoxiainducible, poor, patients, promoter, breast, condition, cocl, mrna, authors, hepatocellular, promotes,

Topics {✒️}

shrna-mediated hif-1α suppression cocl2-induced hif-1α stabilization hypoxia-inducible factor-1alpha correlates transforming growth factor-beta hif-1α sirna pses-hus inducing epithelial-mesenchymal transition stimulates anti-growth signals hypoxia-inducible factor-1 alpha pre-publication history hypoxia-inducible factor-1alpha hypoxia-inducible factor 1alpha e-cadherin-specific repressors snail hypoxia-inducible factor -1α padeasy-hif-1α sirna hif-1alpha promotes metastasis open access article von hippel-landau protein hif-1α mediates repression snail1 induces epithelial full size image active transcription-stimulating complex node-negative breast cancer epithelial mesenchymal transition mesenchymal epithelial transition epithelial-mesenchymal transition mesenchymal-epithelial transition article download pdf hif-1α stabilization potential therapeutic target human breast carcinoma lumophore-conjugated secondary antibodies regulates cell–cell adhesion quantitative real-time pcr reoxygenation-treated hepg2 cells hif-1α activation correlates hif-1α transcriptional regulated g0/g1 arrest hypoxia-inducible factor 1 hypoxia inducible factor-1 hypoxia-inducible factor hif-1α promotes hif-1α negative group cocl2-treated smmc-7721 cells cocl2-pretreated hcc cells hif-1α positive group hif-1α expression profile hif-1α positive samples hypoxia-treated smmc-7721 cells cocl2-treated hcc cells hif-1α promoted

Questions {❓}

• Bidard FC, Pierga JY, Vincent-Salomon A, Poupon MF: A "class action" against the microenvironment: do cancer cells cooperate in metastasis?
• Harrison L, Blackwell K: Hypoxia and anemia: factors in decreased sensitivity to radiation therapy and chemotherapy?

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         headline:Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1α in hepatocellular carcinoma
         description:High invasion and metastasis are the primary factors causing poor prognosis of patients with hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying these biological behaviors have not been completely elucidated. In this study, we investigate the molecular mechanism by which hypoxia promotes HCC invasion and metastasis through inducing epithelial-mesenchymal transition (EMT). The expression of EMT markers was analyzed by immunohistochemistry. Effect of hypoxia on induction of EMT and ability of cell migration and invasion were performed. Luciferase reporter system was used for evaluation of Snail regulation by hypoxia-inducible factor -1α (HIF-1α). We found that overexpression of HIF-1α was observed in HCC liver tissues and was related to poor prognosis of HCC patients. HIF-1α expression profile was correlated with the expression levels of SNAI1, E-cadherin, N-cadherin and Vimentin. Hypoxia was able to induce EMT and enhance ability of invasion and migration in HCC cells. The same phenomena were also observed in CoCl2-treated cells. The shRNA-mediated HIF-1α suppression abrogated CoCl2-induced EMT and reduced ability of migration and invasion in HCC cells. Luciferase assay showed that HIF-1α transcriptional regulated the expression of SNAI1 based on two hypoxia response elements (HREs) in SNAI1 promoter. We demonstrated that hypoxia-stabilized HIF1α promoted EMT through increasing SNAI1 transcription in HCC cells. This data provided a potential therapeutic target for HCC treatment.
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      headline:Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1α in hepatocellular carcinoma
      description:High invasion and metastasis are the primary factors causing poor prognosis of patients with hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying these biological behaviors have not been completely elucidated. In this study, we investigate the molecular mechanism by which hypoxia promotes HCC invasion and metastasis through inducing epithelial-mesenchymal transition (EMT). The expression of EMT markers was analyzed by immunohistochemistry. Effect of hypoxia on induction of EMT and ability of cell migration and invasion were performed. Luciferase reporter system was used for evaluation of Snail regulation by hypoxia-inducible factor -1α (HIF-1α). We found that overexpression of HIF-1α was observed in HCC liver tissues and was related to poor prognosis of HCC patients. HIF-1α expression profile was correlated with the expression levels of SNAI1, E-cadherin, N-cadherin and Vimentin. Hypoxia was able to induce EMT and enhance ability of invasion and migration in HCC cells. The same phenomena were also observed in CoCl2-treated cells. The shRNA-mediated HIF-1α suppression abrogated CoCl2-induced EMT and reduced ability of migration and invasion in HCC cells. Luciferase assay showed that HIF-1α transcriptional regulated the expression of SNAI1 based on two hypoxia response elements (HREs) in SNAI1 promoter. We demonstrated that hypoxia-stabilized HIF1α promoted EMT through increasing SNAI1 transcription in HCC cells. This data provided a potential therapeutic target for HCC treatment.
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      dateModified:2013-03-09T00:00:00Z
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         Epithelial-mesenchymal transition
         Hypoxia
         Hypoxia-inducible factor-1α
         SNAI1
         Hepatocellular carcinoma
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
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      name:Qingliang Wang
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            address:
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               type:PostalAddress
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      name:Jin Zhu
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               type:PostalAddress
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      name:Jiahong Dong
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      name:Department of Radiology, Southwest Hospital, Third Military Medical University, Chongqing, China
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      name:Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China
      name:Institute of Hepatobiliary Surgery, General Hospital of PLA, Beijing, P.R. China
      name:Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China

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