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Last update 08 May 2025

IQGAP1

Last update 08 May 2025

Basic Info

Synonyms

HUMORFA01, IQ motif containing GTPase activating protein 1, IQGAP1

+ [4]

Introduction

Plays a crucial role in regulating the dynamics and assembly of the actin cytoskeleton. Recruited to the cell cortex by interaction with ILK which allows it to cooperate with its effector DIAPH1 to locally stabilize microtubules and allow stable insertion of caveolae into the plasma membrane (By similarity). Binds to activated CDC42 but does not stimulate its GTPase activity. Associates with calmodulin. May promote neurite outgrowth (PubMed:15695813). May play a possible role in cell cycle regulation by contributing to cell cycle progression after DNA replication arrest (PubMed:20883816).

Drugs associated with IQGAP1

NCGC-00138812

Target

CDC42 x IQGAP1

Mechanism

CDC42 inhibitors [+1]

Active Org.

National Institutes of Health

Originator Org.

National Institutes of Health

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MLS-000332963

Target

CDC42 x IQGAP1

Mechanism

CDC42 inhibitors [+1]

Active Org.

National Institutes of Health

Originator Org.

National Institutes of Health

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NCGC00131308

Target

CDC42 x IQGAP1

Mechanism

CDC42 inhibitors [+1]

Active Org.

National Institutes of Health

Originator Org.

National Institutes of Health

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with IQGAP1

100 Translational Medicine associated with IQGAP1

0 Patents (Medical) associated with IQGAP1

741

Literatures (Medical) associated with IQGAP1

01 Jun 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

TNF-α drives bladder cancer metastasis via METTL3-mediated m6A modification to promote CLASP2/IQGAP1-dependent cytoskeleton remodeling

Article

Author: Ou, Zhenyu ; Zhao, Cheng ; He, Cheng ; Chen, Lingxiao

BACKGROUNDBladder cancer (BCa) metastasis is a multi-step process triggered by cytoskeleton reorganization. However, the regulation mechanism of cytoskeleton reorganization in BCa remains ambiguous. This study elucidated the influence of tumor necrosis factor-alpha (TNF-α) in cytoskeleton remodeling during BCa metastasis and its possible mechanisms.METHODSColony formation, scratch, transwell, and the nude mouse model were adopted to evaluate the growth and metastasis. Molecular expression was assessed by immunohistochemical staining, quantitative real-time PCR (qRT-PCR), and Western blotting. The N6-methyladenosine (m6A) level was detected by methylated RNA immunoprecipitation (MeRIP). Protein interaction was validated by Co-immunoprecipitation (Co-IP). Immunofluorescence staining was used to identify rearrangement of actin filament fibers (F-actin) and protein colocalization.RESULTSTNF-α facilitated cytoplasmic linker associated protein 2 (CLASP2) and methyltransferase like 3 (METTL3) expression in a dose (10-50 ng/mL)-dependent manner in BCa. CLASP2 high expression suggested a shorter overall survival of BCa patients. CLASP2 deficiency suppressed BCa cell proliferation, migration, and invasion via disrupting F-actin cytoskeleton. Mechanistically, TNF-α promoted METTL3-mediated m6A modification of CLASP2 to enhance CLASP2 mRNA stability. Moreover, CLASP2 directly interplayed with IQ motif containing GTPase activating protein 1 (IQGAP1) to regulate F-actin cytoskeleton remodeling. In vivo data demonstrated that inhibition of METTL3/CLASP2 axis delayed lung metastasis in nude mice.CONCLUSIONTNF-α favors BCa cell metastasis, which involves METTL3-mediated m6A modification of CLASP2 that interacts with IQGAP1, thus leading to F-actin cytoskeleton remodeling. Our findings suggest targeting TNF-α/METTL3/CLASP2/IQGAP1 axis as a potential avenue for promising treatment for BCa.

01 Apr 2025·Journal of Orthopaedic Research

A Novel Disulfidptosis‐Related Risk Signature for Prognostic Prediction in Patients With Ewing Sarcoma

Article

Author: Che, Chunqing ; Song, Delei ; Yin, Xuqing ; Xue, Peng

ABSTRACTEwing sarcoma (ES) is a malignant bone tumor prevalent among children and adolescents. Disulfidptosis represents a novel form of cell death; however, the mechanism of disulfidptosis in ES remains unclear. Our aim is to explore the disulfidptosis‐related prognostic signature in ES. Utilizing transcriptomic and clinical data of ES, disulfidptosis‐related hub genes (DRHGs) were identified by differential gene expression analysis and Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression analysis. A disulfidptosis‐related risk score model (DRRS) was constructed based on these DRHGs. The performance of DRRS was assessed using survival analysis and receiver operating characteristic curve analysis. Immune cell infiltration in different risk subgroups and correlations between DRRS and antitumor reagents were also analyzed. In this study, we developed a disulfidptosis‐related prognostic feature based on LRPPRC (leucine rich pentatricopeptide repeat containing), IQGAP1 (IQ motif containing GTPase activating protein 1), NDUFS1 (NADH:ubiquinone oxidoreductase core subunit S1), and TLN1 (talin 1), which may serve as a predictive and independent risk factor for ES. ES patients in the high‐risk group exhibited a poorer prognosis, had a higher proportion of myeloid‐derived suppressor cells (MDSCs) and M2 type of tumor‐associated macrophages, and showed heightened sensitivity to some antitumor agents such as nilotinib and olaparib. This study is the first to construct a disulfidptosis‐related prognostic signature that may predict the prognosis and immune response in ES patients, thereby providing a new reference for understanding the mechanisms of ES and guiding immunotherapy.

01 Apr 2025·The FEBS Journal

Pannexin 1 crosstalk with the Hippo pathway in malignant melanoma

Article

Author: Li, Zhigang ; Sayedyahossein, Samar ; Huang, Kenneth ; Penuela, Silvia ; Karimi, Mehdi ; Dagnino, Lina ; O'Donnell, Brooke L. ; Johnston, Danielle ; Leighton, Stephanie E. ; Bahmani, Mehrnoosh ; Huver, Matthew S. ; Sacks, David B. ; Zhang, Christopher ; Wakefield, Brent

In this study, we explored the intricate relationship between Pannexin 1 (PANX1) and the Hippo signaling pathway effector, Yes‐associated protein (YAP). Analysis of The Cancer Genome Atlas (TCGA) data revealed a significant positive correlation between PANX1 mRNA and core Hippo components, Yes‐associated protein 1 [YAP], Transcriptional coactivator with PDZ‐binding motif [TAZ], and Hippo scaffold, Ras GTPase‐activating‐like protein IQGAP1 [IQGAP1], in invasive cutaneous melanoma and breast carcinoma. Furthermore, we demonstrated that PANX1 expression is upregulated in invasive melanoma cell lines and is associated with increased YAP protein levels. Notably, our investigations uncovered a previously unrecognized interaction between endogenous PANX1 and the Hippo scaffold protein IQGAP1 in melanoma cells. Moreover, our findings revealed that IQGAP1 exhibits differential expression in melanoma cells and plays a regulatory role in cellular morphology. Functional studies involving PANX1 knockdown provided compelling evidence that PANX1 modulates YAP protein levels and its cotranscriptional activity in melanoma and breast carcinoma cells. Importantly, our study highlights the potential therapeutic significance of targeting PANX1. Pharmacological inhibition of PANX1 using selective FDA‐approved inhibitors or PANX1 knockdown reduced YAP levels in melanoma cells. Furthermore, our Clariom™ S analysis unveiled key genes implicated in cell proliferation, such as neuroglin1 (NRG1), β‐galactoside binding protein and galectin‐3 (LGALS3), that are affected in PANX1‐deficient cells. In summary, our investigation delves into the intricate interplay between PANX1 and YAP in the context of invasive melanoma, offering valuable insights into potential therapeutic strategies for effective treatment.

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