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@# Objective: To explore the expression of IQGAP1 (Ras GTPase-activating-like protein containing IQ domain) in esophageal squamous cell carcinoma (ESCC) tissues and cell lines and its effect on the proliferation and invasion of TE-2 cell. Methods: Totally 125 pairs of cancer tissues and para-cancerous tissues from ESCC patients, who underwent surgical resection inAffiliated Tumor Hospital of Zhengzhou University from January 2015 to December 2016, were included in this study; in addition, ESCC cell lines (TE-2, TE3, ECA109) and normal esophageal epithelial cell line Het-1A were also collected. The expression of IQGAP1 was detected by immunohistochemical staining and its relationship with cliniopathological features was also analyzed. IQGAP1 mRNA and protein expressions in ESCC cell lines were detected by Real-time quantitative PCR (qPCR) and Western blotting, respectively. TE-2 cells were transfected with si-IQGAP1 (positive transfection group) and si-CTRL (negative control group) plasmids, and the effects of IQGAP1 silencing on the proliferation and invasion of TE-2 cells were detected by MTT and Transwell assay. The expressions of E-cadherin and Ncadherin were detected by Western blotting. Results: The positive expression rate of IQGAP1 in ESCC tissues was significantly higher than that in para-cancerous tissues (P<0.05), which was closely related to tumor stage and histologic grade (all P<0.05). The mRNAand protein expressions of IQGAP1 in TE-2, TE-3 and ECA109 cells were significantly higher than those in Het-1Acells (all P<0.05).After IQGAP1 was silenced, compared with the negative control group and the blank group, the expression of IQGAP1 mRNAand protein in the positive transfection group significantly decreased (all P<0.05); the proliferation and invasiveness of TE-2 cells significantly decreased (all P<0.05); E-cardherin was up-regulated while N-cardherin was down-regulated (all P<0.05) in the positive interference group. Conclusion: IQGAP1 is highly expressed in ESCC tissues, and si-IQGAP1 can inhibit the proliferation and invasion of TE-2 cells, which plays an important role in the occurrence and development of ESCC.
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Objective:To examine the expression of IQGAP1 in hepatocellular carcinoma and its effect on vasculogenic mimicry(VM). Methods:Immunohistochemical staining was performed to investigate the expression of IQGAP1.CD31/PAS double staining was per-formed to detect VM and analyze the correlation of IQGAP1 and VM.HepG2 cells were transfected with an IQGAP1 overexpression plasmid to induce exogenous expression of IQGAP1,and an IQGAP1 knockdown plasmid was transfected into SMMC7721 cells to re-duce IQGAP1 levels.The expression of cancer stem cell markers CD133,CD44,Sox2,and ALDH1 was analyzed by Western blot and compared with that in the control.Cellular functional experiments were used to determine the role of IQGAP1 in promoting cancer cells' ability of invasiveness and migration, proliferation, and VM formation. Results: Immunohistochemical analysis revealed that IQGAP1 was mainly located in the cell membrane and/or cytoplasm,and the staining intensity was correlated with tumor grade,me-tastasis,and VM(P<0.05).Cells transfected with the overexpression plasmid showed enhanced CD133,CD44,Sox2,and ALDH1 levels due to the increase in IQGAP1 and exhibited increased invasion ability,proliferation,and VM formation.In the SMMC7721 cells trans-fected with the knockdown plasmid,CD133,CD44,Sox2,and ALDH1 levels were decreased and motility was inhibited.Conclusions:IQGAP1 supports malignant behavior in hepatocellular carcinoma and may promote VM by increasing stemness.
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Sepsis is one of the main cause of patients' death. Lung is the most vulnerable target organ during sepsis, and sepsis patients are often complicated with acute respiratory distress syndrome (ARDS), of which the main mechanism is vascular leakage caused by cytoskeleton rearrangement and cell-to-cell connection changes. IQ-guanosine triphosphatease-activating protein 1 (IQGAP1) has become the key component of cytoskeleton dynamics regulation in recent years. At present, the relationship between IQGAP1 and ARDS induced by sepsis is not yet clear. In this article, we will review the mechanism of the interaction between IQGAP1 and pathogenic microorganisms, changes of pulmonary micro vascular barrier function and cyto-skeleton at the molecular level.
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Objective:To study the expression of IQ motif containing GTPase activating protein 1 (IQGAP1 )in oral squamous cell cancer(OSCC)tissue,and to explore the effects of IQGAP1 on cell proliferation and invasion as well as its underlying mechanism. Methods:Expression levels of IQGAP1 in tumor and adjacent normal tissues were examined by western blot and RT-PCR.OSCC cell line SCC-4 cells was transfected with the recombinant plasmid-pcDNA3.1 -IQGAP1 by lipofectamine,and then treated with an Akt in-hibitor.The phosphorylation of Akt,cell proliferation and invasion were detected by western blot,MTT assay and Transwell invasion as-say respectively.Results:Protein and mRNA expression levels of IQGAP1 were higher in cancer tissue than in adjacent normal tissue (P <0.05).Transfection of pcDNA3.1 -IQGAP1 increased IQGAP1 expression,enhanced the capability of cell proliferation and inva-sion (P <0.05),increased p Akt level in the cells.Preconditioning with an Akt inhibitor reduced p Akt level.Furthermore,silencing Akt pathway blocked the increase of cell proliferation and invasion induced by IQGAP1 overexpression(P <0.05).Conclusion:IQ-GAP1 overexprission can mediate the ability of proliferation and invasion of OSCC cells by regulating the activation of Akt pathway.
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IQGAP1 is a scaffold protein which binds to various signaling and structural molecules.By interacting with target proteins,IQGAP1 participates in integration of signaling pathways and regulation of cellular functions.More and more evidences suggest that IQGAP1 plays an important role in tumorigenesis by promoting cell proliferation and transformation,weakening cell adhesion and stimulating cell motility and invasion.