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c-myc suppresses microrna-29b month download article/chapter real-time quantitative pcr epithelial-stromal cross-talk epithelial-mesenchymal transition mir-26b-5p expression suppress tumor growth targeting pi3k/akt pathway tumor angiogenic factor cutaneous malignant melanoma—implications human ovarian carcinoma—role full article pdf mir-26b-5p microrna-26b suppresses suppressing mir-29b mesenchymal transition privacy choices/manage cookies hubler jr wr hepatocellular carcinoma cells regulating cell cycle human liver cancers downregulating jun expression downregulating rock1 expression mature mir-26 family related subjects cell cycle progression human melanoma cells article wang mir-1285-3p acts tube formation abilities tube formation ability microvessel density compared promote drug resistance promote tumor aggressiveness high tumor grade mol cancer ther human skin tumors mol cell biol human breast cancer cancer biol ther vascular channel formation hcc remains unknown huaier suppresses proliferation european economic area dimensional culture assays agosto-perez fj ethics declarations conflicts electronic supplementary material tumor cell metastasis bmc cancer

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         headline:Regulation of proliferation, angiogenesis and apoptosis in hepatocellular carcinoma by miR-26b-5p
         description:MicroRNAs (miRNAs) play vital roles in cell proliferation, differentiation and apoptosis in hepatocellular carcinoma (HCC). miR-26b has been confirmed as an important regulator in carcinogenesis and other pathological processes. miR-26b-5p is one member of the mature miR-26 family, and its functional role in proliferation, angiogenesis and apoptosis in HCC remains unknown. Here, we demonstrate that miR-26b-5p expression was significantly decreased in HCC tissues and HCC cell lines compared with normal liver tissues and liver cells by quantitative real-time polymerase chain reaction (qRT-PCR). The relationships between miR-26b-5p and the clinical characteristics of HCC patients were further analysed, and miR-26b-5p was positively correlated with the differentiation of HCC cells. Computational searches were further used to identify the downstream targets and signalling pathways of miR-26b-5p in HCC cells. Cell viability, proliferation and tube formation abilities were assessed by scrape, 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and three-dimensional culture assays to confirm that miR-26b-5p inhibited HCC cell growth and impaired the tube formation ability of the HCC cells. Both in vitro and in vivo studies showed that miR-26b-5p could suppress vascular mimicry (VM) and angiogenesis by down-regulating the expression of VE-cadherin, Snail and MMP2 and could inhibit the apoptosis of HCC cells. Using mouse models, we revealed that tumours derived from miR-26b-5p-expressing HCC cells displayed a significant decrease in microvessel density compared with those derived from control cells. Therefore, our data provide further insight into the role of miR-26b-5p as a negative regulator of proliferation, angiogenesis, and apoptosis in HCC.
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      description:MicroRNAs (miRNAs) play vital roles in cell proliferation, differentiation and apoptosis in hepatocellular carcinoma (HCC). miR-26b has been confirmed as an important regulator in carcinogenesis and other pathological processes. miR-26b-5p is one member of the mature miR-26 family, and its functional role in proliferation, angiogenesis and apoptosis in HCC remains unknown. Here, we demonstrate that miR-26b-5p expression was significantly decreased in HCC tissues and HCC cell lines compared with normal liver tissues and liver cells by quantitative real-time polymerase chain reaction (qRT-PCR). The relationships between miR-26b-5p and the clinical characteristics of HCC patients were further analysed, and miR-26b-5p was positively correlated with the differentiation of HCC cells. Computational searches were further used to identify the downstream targets and signalling pathways of miR-26b-5p in HCC cells. Cell viability, proliferation and tube formation abilities were assessed by scrape, 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and three-dimensional culture assays to confirm that miR-26b-5p inhibited HCC cell growth and impaired the tube formation ability of the HCC cells. Both in vitro and in vivo studies showed that miR-26b-5p could suppress vascular mimicry (VM) and angiogenesis by down-regulating the expression of VE-cadherin, Snail and MMP2 and could inhibit the apoptosis of HCC cells. Using mouse models, we revealed that tumours derived from miR-26b-5p-expressing HCC cells displayed a significant decrease in microvessel density compared with those derived from control cells. Therefore, our data provide further insight into the role of miR-26b-5p as a negative regulator of proliferation, angiogenesis, and apoptosis in HCC.
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      name:Fang Liu
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Bing Shao
      affiliation:
            name:Tianjin Medical University
            address:
               name:Department of Pathology, Tianjin Medical University, Tianjin, China
               type:PostalAddress
            type:Organization
      name:Jindan An
      affiliation:
            name:Mudanjiang Medical University
            address:
               name:Department of Pathology, Mudanjiang Medical University, Heilongjiang, China
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology and Cancer Hospital and General Hospital of Tianjin, Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin General Hospital, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Tianjin Medical University, Tianjin, China
      name:Department of Pathology, Mudanjiang Medical University, Heilongjiang, China
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