The IQGAP3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the IQGAP3 gene in the HeLa cell background. This polyclonal pool provides a heterogeneous loss-of-function model without clonal isolation, enabling functional studies of IQGAP3 in a human cervical adenocarcinoma context. The population carries CRISPR/Cas9-mediated gene disruption, creating a versatile tool for investigating IQGAP3-dependent signaling and cellular behaviors.
The host HeLa cell line is an immortalized human cervical adenocarcinoma epithelial line, originally isolated from Henrietta Lacks in 1951. HeLa cells are HPV18-positive and widely employed as a model for cancer biology, including studies of cell cycle regulation, apoptosis, and tumorigenesis. Their robust growth and well-characterized signaling networks make HeLa a standard platform for gene-edited cell products aimed at dissecting oncogenic mechanisms.
IQGAP3 functions as a scaffold protein that orchestrates actin cytoskeleton dynamics, cell migration, and proliferation. It directly interacts with small GTPases Rac1 and Cdc42, linking them to downstream effectors such as N-WASP and the Arp2/3 complex to promote actin polymerization. IQGAP3 also integrates Wnt/??-catenin signaling by associating with ??-catenin, APC, and E-cadherin, thereby modulating TCF-mediated transcription of cyclin D1. Upstream, IQGAP3 is activated by EGF/EGFR and TGF-?? pathways through ERK1/2 and Akt phosphorylation, while its expression is transcriptionally regulated by c-Myc and STAT3. In HeLa polyclonal knockout cells, loss of IQGAP3 attenuates these signaling axes, leading to reduced ERK and cyclin D1 levels, impaired actin reorganization, and compromised gap junction assembly and mitosis.
Given the host HeLa cell??s origin from cervical carcinoma and IQGAP3??s established overexpression in multiple malignancies??including colorectal, breast, gastric, and cervical cancers??this knockout model is particularly relevant for studying metastatic behavior and poor prognosis mechanisms. The polyclonal population captures the heterogeneity of gene disruption events, reflecting the diversity of loss-of-function effects that may occur in tumor cell populations. Researchers can employ this model to investigate how IQGAP3 loss impacts cell motility, invasion, and proliferation in the context of cervical cancer and beyond, providing insights into its role as a potential therapeutic target.
Typical applications of IQGAP3 Knockout HeLa Polyclonal Cells include cancer cell migration and invasion assays (e.g., scratch wound healing, Transwell migration/invasion), Wnt/??-catenin signaling studies, cytoskeletal dynamics research, and cell cycle/proliferation analyses using MTT or flow cytometry. These cells are also suited for co-immunoprecipitation and immunofluorescence experiments to examine protein interactions and F-actin distribution. Downstream signaling can be assessed by Western blotting for ERK, Akt, and cyclin D1, or by RT-qPCR for ??-catenin target genes. This product serves as a flexible loss-of-function tool for dissecting IQGAP3-mediated pathways in oncogenic contexts. For further information, please contact Ascent Research.
