SUMOylation of IQGAP1 promotes the development of colorectal cancer

Liang, Ziwei; Yang, Yanfei; He, Yu; Yang, Pengbo; Wang, Xixi; He, Gu; Zhang, Peng; Zhu, Hongxia; Xu, Nuo; Zhao, Xia

doi:10.1016/j.canlet.2017.09.046

Cited by 42 publications

(56 citation statements)

References 48 publications

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“…It is supported by various literature [19]. SUMOylation on IQGAP1 affects the development of colorectal cancer [20], and IQGAP1 promotes CRC cell growth, migration, and tumorigenesis by activating the phosphorylation of ERK, MEK, and AKT. The mechanism of SUMOylation in IQGAP1, especially its binding sites, is still unclear and requires more study and better methods to yield absolute results.…”

Section: Introductionmentioning

confidence: 68%

In Silico Study of Mirna-Regulated Iq Motif-Containing Gtpase-Activating Protein Family in Liver Cancer

Agustriawan

Sumarpo

Parikesit

et al. 2018

Asian J Pharm Clin Res

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Objective: The aim of this paper is to identify the list of microRNA (miRNA) which can regulate the aberrant expression of IQGAP in liver cancer formation. The aberrant expression of IQ motif-containing GTPase-activating protein (IQGAP) family which consists of IQGAP1, IQGAP2, and IQGAP3 has been linked to carcinogenesis in human cancers. The reciprocal expression of IQGAP family in human cancer has been studied to act as oncogenes or tumor suppressor genes. A growing number of studies suggest that upregulated or downregulated expression of IQGAP family triggers cancer development.Methods: A correlation study was performed to construct a pathway to inhibit or activate IQGAP family between miRNAs and IQGAPs. A pre-processing step was conducted to download, filter and process the dataset from TCGA. It yields miRNA and IQGAP gene expression matrix. Then, correlation computation was computed using MATLAB. Moreover, this study linked the results to the MiRTarBase to validate the prediction result with the wet lab experimental result.Results: This study identified significantly inversely correlation in 51 miRNAs-IQGAP1, 169 miRNAs-IQGAP2, and 33 miRNAs-IQGAP3, respectively, which may potentially play a role in a liver cancer formation. Some of the results also can be found in miRTarBase. It supports the precision of those miRNA and IQGAP interaction between dry lab and wet lab study. IQGAP1 and IQGAP2 mostly has been identified as an oncogene in cancer but IQGAP2 has been discovered as tumor suppressor gene. The list of miRNA in the result of this study can become a potential therapy to target the aberrant expression of IQGAP family.Conclusion: miRNA function is known as an oncogene or tumor suppressor gene in cancer development. Therefore, it can be one of the important molecular biology which may target the aberrant expression of IQGAP in liver cancer.

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Section: Introductionmentioning

confidence: 68%

In Silico Study of Mirna-Regulated Iq Motif-Containing Gtpase-Activating Protein Family in Liver Cancer

Agustriawan

Sumarpo

Parikesit

et al. 2018

Asian J Pharm Clin Res

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“…Cell viability. Cell viability was measured by CCK-8 assay as previously described (30). The OS-RC-2 and 786-O cells were seeded on a 6-well plate and incubated with 50 nM siPGRMC1 or siNC per well.…”

Section: Methodsmentioning

confidence: 99%

“…Cell migration. Cell migration was detected within a 24-well Transwell chamber system (PIEP12R48; EMD Millipore, Billerica, MA, USA) (28)(29)(30). The OS-RC-2 and 786-O cells were seeded on a 6-well plate for incubation with 50 nM siPGRMC1 or siNC per well.…”

Section: Methodsmentioning

confidence: 99%

Combined assessment of low PGRMC1/positive ATP1A1 levels has enhanced prognostic value for renal cell carcinoma

Zhang

et al. 2018

Oncol Rep

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Progesterone receptor membrane component 1 (PGRMC1) and Na+/K+‑ATPase α1 subunit (ATP1A1) are two proteins associated with the clinical prognosis of renal cell carcinoma (RCC) and RCC cell proliferation. However, the two proteins have been previously studied independently, and their combined influence on the clinical outcome of RCC remains unclear. The present study suggests that the combined expression levels of PGRMC1 and ATP1A1 (PGRMC1/ATP1A1) are associated with the clinical prognosis of RCC patients. RCC patients with low PGRMC1/positive ATP1A1 levels exhibited the best overall survival (OS) outcomes (103.08±1.85 months). The high PGRMC1/negative ATP1A1 group demonstrated the worst prognosis (73.1±8.87 months). The low PGRMC1/positive ATP1A1 group had the highest 7‑year OS rate (92.3%). The high PGRMC1/negative ATP1A1 group had the lowest 7‑year OS rate (46.7%). Although PGRMC1 and ATP1A1 both act on AKT phosphorylation in RCC cells, their expression levels are independent of each other. Moreover, the synergistic suppressive roles of PGRMC1 downregulation combined with ATP1A1 upregulation exhibit more efficient tumor inhibition potentials on RCC cells. Therefore, combined assessment of the two biomarkers (PGRMC1/ATP1A1) shows enhanced prognostic ability for RCC.

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“…IQGAP1 interacts with pro-tumorigenic processes, including kinase signaling, cell proliferation, motility, and adhesion [10]. Furthermore, in vivo studies demonstrate that increased IQGAP1 expression can promote tumor growth, indicating that IQGAP1 could be an effective molecular target for HCC [15][16][17]. Yet, other studies revealed that deletion of IQGAP1 in cancer cells and/or stromal cells can also enhance tumorigenesis by modulating transforming growth factor (TGF) signaling [18,19] and adherens junction stability [20].…”

Section: Introductionmentioning

confidence: 99%

Deletion and overexpression of the scaffolding protein IQGAP1 promotes HCC

Delgado

Erickson

Tao

et al. 2020

Preprint

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IQ motif-containing GTPase-activating protein 1 (IQGAP1) is a ubiquitously expressed scaffolding protein that is overexpressed in a number of cancers, including liver cancer, and is associated with many pro-tumorigenic processes including cell proliferation, motility, and adhesion. IQGAP1 can integrate multiple signaling pathways and could be an effective antitumor target. Therefore, we examined the role for IQGAP1 in tumor initiation and promotion during liver carcinogenesis. Unexpectedly, we found that Iqgap1 -/mice had a higher tumor burden than Iqgap1 +/+ and Iqgap1 +/mice following DEN-induced liver carcinogenesis. Iqgap1 -/tumors as well as knocking down IQGAP1 in hepatocellular carcinoma (HCC) cell lines resulted in increased MET activation and cellular proliferation. On the other hand, we uncovered IQGAP1 overexpression accelerates HCC development by YAP activation and subsequent NUAK2 expression. We demonstrate that increasing IQGAP1 expression in vivo does not alter β-catenin or MET activation. Taken together, we identify that both loss and gain of function of IQGAP1 promotes HCC development by two separate mechanisms in the liver. These results demonstrate that adequate amount of IQGAP1 is necessary to maintain a quiescent status of liver.

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SUMOylation of IQGAP1 promotes the development of colorectal cancer

Cited by 42 publications

References 48 publications

In Silico Study of Mirna-Regulated Iq Motif-Containing Gtpase-Activating Protein Family in Liver Cancer

In Silico Study of Mirna-Regulated Iq Motif-Containing Gtpase-Activating Protein Family in Liver Cancer

Combined assessment of low PGRMC1/positive ATP1A1 levels has enhanced prognostic value for renal cell carcinoma

Deletion and overexpression of the scaffolding protein IQGAP1 promotes HCC

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