IQGAP1 and IGFBP2

McDonald, Kerrie L.; O'Sullivan, Maree; Parkinson, Jonathan; Shaw, Janet M.; Payne, Cathy A.; Brewer, Janice; Young, Lawrence S.; Reader, Dianne J.; Wheeler, Helen; Cook, Raymond; Biggs, Michael T.; Little, Nicholas; Teo, Charlie; Stone, Graham N.; Robinson, Bruce G.

doi:10.1097/nen.0b013e31804567d7

Cited by 85 publications

(30 citation statements)

References 35 publications

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“…Although an increasing number of studies has aimed to elucidate the expression of IQGAP1 in various types of cancer, including lung cancer (21), endometrial cancer (22), ovarian cancer (23), gastric cancer (24), colon cancer (25), hepatic carcinoma (26), breast cancer (27) and even glioma (28), the molecular roles of IQGAP1 remain to be understood and the correlation between clinical outcomes and IQGAP1 expression in human malignant tumors require further investigation. The present study indicated that IQGAP1-siRNA inhibited the proliferation and metastasis of U251 and U373 glioma cells.…”

Section: Discussionmentioning

confidence: 99%

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IQGAP1-siRNA inhibits proliferation and metastasis of U251 and U373 glioma cell lines

Diao

Liu

Zhang

et al. 2017

Molecular Medicine Reports

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IQ motif containing GTPase activating protein 1 (IQGAP1) is a scaffold protein, which is aberrantly expressed in several tumor types and is closely associated with the development, metastasis and prognosis of cancer. Several studies have demonstrated that IQGAP1 has broad prospects in the basic and clinical research of tumors. The present study aimed to explore the effects of IQGAP1-small interfering (si) NA on the proliferation and metastasis of U251 and U373 glioma cell lines, which markedly expressed IQGAP1. The human glioma cell lines (U251 and U373) were transfected with siRNA and transfection efficacy was confirmed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. Cell proliferation was detected using the Cell Counting kit-8, and cell metastasis capabilities were detected using cell adhesion, migration and invasion assays. In addition, the expression levels of several tumor-associated genes were determined by RT-qPCR and western blotting. The results indicated that IQGAP1 was expressed at higher levels in glioma tissues compared with in normal brain tissues. IQGAP1-siRNA significantly inhibited cell proliferation, and cell adhesion, migration and invasion. Furthermore, the expression levels of matrix metalloproteinase (MMP)2, Snail, MMP9, fibronectin 1 and Twist were suppressed, and E-cadherin was upregulated in response to siRNA-IQGAP1. The present study identified the function of IQGAP1 in glioma cell biology, and indicated that it may be considered a novel target for glioma treatment.

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Section: Discussionmentioning

confidence: 99%

“…With regards to glioma, patients with glioblastoma and negative IQGAP1 expression have been reported to survive for >3 years (28). Studies regarding the effects of IQGAP1 on cell proliferation are increasing.…”

Section: Discussionmentioning

confidence: 99%

IQGAP1-siRNA inhibits proliferation and metastasis of U251 and U373 glioma cell lines

Diao

Liu

Zhang

et al. 2017

Molecular Medicine Reports

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“…IQGAP1 could impair the intrinsic GTPase activity of CDC42, thus stabilizing CDC42 in its activated form [34]. IQGAP1 was detected to be highly expressed in several cancer types, and resulted in poor prognosis and survival of patients [35,36,37]. As an effector of CDC42, IQGAP1 can bind directly to CDC42 and has been implicated in the modulation of cell architecture and regulation of exocytosis in human cancers.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B Virus X Protein Stimulates Proliferation, Wound Closure and Inhibits Apoptosis of HuH-7 Cells via CDC42

Luo

et al. 2017

IJMS

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Chronic hepatitis B virus (HBV) infection has been considered as the major cause of hepatocellular carcinoma (HCC). Hepatitis B virus X protein (HBx) has been reported to be oncogenic. The underlying mechanisms of HBV-related HCC are not fully understood, and the role played by the HBx protein in HBV induced carcinogenesis remains controversial. CDC42, a member of the Rho GTPase family, has been reported to be overexpressed in several different cancers, including HBV-related HCC. However, the specific role of CDC42 in HCC development remains unclear. Here, we investigated the cellular mechanisms by which CDC42 was responsible for the higher proliferation of HuH-7 cells mediated by HBx. We found that the expression level of CDC42 and its activity were significantly increased in HuH-7-HBx cells. The deficiency of CDC42 using the CRISPR/Cas9 system and inhibition by specific inhibitor CASIN led to the reduction of HBx-mediated proliferation. Furthermore, we observed that IQ Motif Containing GTPase Activating Protein 1 (IQGAP1), the downstream mediator of the CDC42 pathway, might be involved in the carcinogenesis induced by HBx. Therefore, the HBx/CDC42/IQGAP1 signaling pathway may potentially play an important role in HBx-mediated carcinogenesis.

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“…Moreover, IGFBP-2 is significantly associated with the Ki-67 labeling index in gastric carcinoma 55. In addition, over the past 15 years, results of several studies reporting increased expression of IGFBP-2 have correlated it with poor clinical GBM patient outcomes 56–59. Moreover, recent studies have reported that plasma IGFBP-2 levels could predict the clinical outcomes of GBM patients 25,60,61.…”

Section: Discussionmentioning

confidence: 99%

<em>FBLN4</em> as candidate gene associated with long-term and short-term survival with primary glioblastoma

Li¹,

Li²,

Zhang³

et al. 2017

OTT

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BackgroundGlioblastoma multiforme (GBM) is the most common malignant and lethal type of primary central nervous system tumor in humans. In spite of its high lethality, a small percentage of patients have a relatively good prognosis, with median survival times of 36 months or longer. The identification of clinical subsets of GBM associated with distinct molecular genetic profiles has made it possible to design therapies tailored to treat individual patients.MethodsWe compared microarray data sets from long-term survivors (LTSs) and short-term survivors (STSs) to screen for prognostic biomarkers in GBM patients using the WebArrayDB platform. We focused on FBLN4, IGFBP-2, and CHI3L1, all members of a group of 10 of the most promising, differentially regulated gene candidates. Using formalin-fixed paraffin-embedded GBM samples, we corroborated the relationship between these genes and patient outcomes using methylation-specific polymerase chain reaction (PCR) for MGMT methylation status and quantitative reverse transcription PCR for expression of these genes.ResultsExpression levels of the mRNAs of these 3 genes were higher in the GBM samples than in normal brain samples and these 3 genes were significantly upregulated in STSs compared to the levels in LTS samples (P<0.01). Furthermore, Kaplan–Meier analysis showed that the expression patterns of FBLN4 and IGFBP-2 serve as independent prognostic indicators for overall survival (P<0.01 and P<0.05, respectively).ConclusionTo our knowledge, this is the first report describing FBLN4 as a prognostic factor for GBM patient survival, demonstrating that increased GBM survival time correlates with decreased FBLN4 expression. Understanding FBLN4 expression patterns could aid in the creation of powerful tools to predict clinical prognoses of GBM patients.

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IQGAP1 and IGFBP2

Cited by 85 publications

References 35 publications

IQGAP1-siRNA inhibits proliferation and metastasis of U251 and U373 glioma cell lines

IQGAP1-siRNA inhibits proliferation and metastasis of U251 and U373 glioma cell lines

Hepatitis B Virus X Protein Stimulates Proliferation, Wound Closure and Inhibits Apoptosis of HuH-7 Cells via CDC42

<em>FBLN4</em> as candidate gene associated with long-term and short-term survival with primary glioblastoma

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