Blockade of ARHGAP11A reverses malignant progress via inactivating Rac1B in hepatocellular carcinoma

• DOI: 10.1186/s12964-018-0312-4
• Publication Date: 2018-12-13T13:38:36Z
• Authors: Bin Dai; Xuan Zhang; Runze Shang; Jianlin Wang; Xisheng Yang; Hong Zhang; Qi Liu; Desheng Wang; Lin Wang; Kefeng Dou
• Keywords: Male; rac1 GTP-Binding Protein; 0301 basic medicine; Carcinoma, Hepatocellular; Epithelial-Mesenchymal Transition; Hepatocellular carcinoma; Metastasis; 03 medical and health sciences; Cell Movement; Cell Line, Tumor; Humans; Neoplasm Invasiveness; Neoplasm Metastasis; Cell Proliferation; Rac1B; QH573-671; Research; GTPase-Activating Proteins; Liver Neoplasms; EMT; R; Middle Aged; ARHGAP11A; 3. Good health; Gene Expression Regulation, Neoplastic; Cell Transformation, Neoplastic; Gene Knockdown Techniques; Disease Progression; Medicine; Female; Cytology

The molecular signaling events involving in high malignancy and poor prognosis of hepatocellular carcinoma (HCC) are extremely complicated. Blockade currently known targets has not yet led to successful clinical outcome. More understanding about the regulatory mechanisms HCC is necessary for developing new effective therapeutic strategies patients. expression Rho GTPase-activating protein 11A (ARHGAP11A) was examined human normal liver tissues. correlations between ARHGAP11A clinicopathological stage or patients were analyzed. downregulated determine its role proliferation, invasion, migration, epithelial-to-mesenchymal transition (EMT) development, cells vitro vivo. exhibited HCC, significantly correlated with Moreover, facilitated Hep3B MHCC97-H cell migration EMT development vitro. knockdown inhibited vivo growth metastasis cells. Furthermore, directly interacted Rac1B independent GTPase- activating activity. blockade effectively interrupted ARHGAP11A-elicited malignant phenotype. Meanwhile, upregulation reversed mediated mesenchymal-to-epithelial (MET) facilitates progression via ARHGAP11A-Rac1B interaction. ARHGAP11A/Rac1B could be a potential target treatment HCC.