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10.7150/thno.25166

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suck abstract from ncbi


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pmid30026878
      Theranostics 2018 ; 8 (13 ): 3707-3721
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  • AP-2? inhibits hepatocellular carcinoma invasion and metastasis through Slug and Snail to suppress epithelial-mesenchymal transition #MMPMID30026878
  • Yang L ; Qiu J ; Xiao Y ; Hu X ; Liu Q ; Chen L ; Huang W ; Li X ; Li L ; Zhang J ; Ding X ; Xiang S
  • Theranostics 2018[]; 8 (13 ): 3707-3721 PMID30026878 show ga
  • Transcription factor AP-2? plays an important role in human cancer, but its clinical significance in hepatocellular carcinogenesis is largely unknown. Methods: AP-2? expression was detected in human hepatocellular cancer (HCC) tissues and cell lines. The effects of AP-2? on HCC proliferation, migration, invasion, tumor formation and metastasis were evaluated by MTT, colony formation and transwell assays in vitro and mouse experiments in vivo. The association between AP-2? and miR-27a/EMT markers in HCC cell lines and tissues was analyzed. Results: AP-2? expression was decreased in HCC tissues and cell lines. Reduced expression of AP-2? was significantly associated with more advanced tumor stages and larger tumor sizes. The overexpression of AP-2? reduced HCC proliferation, migration, invasion, tumor formation and metastasis in vitro and in vivo. Additionally, AP-2? overexpression increased the sensitivity of HCC cells to cisplatin. Moreover, AP-2? modulates the levels of EMT markers through Slug and Snail in HCC cell lines and tissues. Furthermore, oncogenic miR-27a inhibits AP-2? expression by binding to the AP-2? 3' untranslated region (UTR) and reverses the tumor suppressive role of AP-2?. Conclusion: These results suggested that AP-2? is lowly expressed in HCC by inhibiting EMT signaling to regulate HCC cell growth and migration. Therefore, AP-2? in the novel miR-27a/AP-2?/Slug/EMT regulatory axis enhances the chemotherapeutic drug sensitivity of HCC and might represent a potential target for evaluating the treatment and prognosis of human HCC.
  • |*Carcinogenesis [MESH]
  • |*Epithelial-Mesenchymal Transition [MESH]
  • |*Neoplasm Metastasis [MESH]
  • |Animals [MESH]
  • |Carcinoma, Hepatocellular/pathology/*physiopathology [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Movement [MESH]
  • |Cell Proliferation [MESH]
  • |Disease Models, Animal [MESH]
  • |Humans [MESH]
  • |Mice [MESH]
  • |Models, Biological [MESH]
  • |Neoplasm Invasiveness [MESH]
  • |Snail Family Transcription Factors/*metabolism [MESH]


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