The ACTR3C Knockout HeLa Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of HeLa cells designed for targeted disruption of the human ACTR3C gene. This loss-of-function model yields a heterogeneous pool of knockout cells, enabling population-level studies of ACTR3C function without the constraints of clonal selection. The polyclonal format is advantageous for assays requiring robust biological replicates and reduced clone-specific artifacts.
The parental HeLa cell line is a widely used immortalized cervical adenocarcinoma epithelial line, originating from Henrietta Lacks. HeLa cells harbor human papillomavirus 18 (HPV-18) sequences that cause inactivation of the tumor suppressors p53 and retinoblastoma protein (Rb), creating a background of genomic instability and uncontrolled proliferation that mirrors many aspects of human cancers.
ACTR3C encodes an actin-related protein that participates in both cytoplasmic and nuclear actin dynamics. In the cytoplasm, ACTR3C is involved in actin filament nucleation by interacting with ARP2/3 complex subunits and actin monomers downstream of Rho family GTPases, including Rac1 and RhoA. These GTPases are activated by growth factor receptors such as EGFR and PDGFR. In the nucleus, ACTR3C associates with chromatin remodeling complexes like SWI/SNF and influences chromatin structure and DNA repair processes, potentially bridging extracellular signals to genomic regulation. Representative pathway components include Rac1, RhoA, ARP2/3, WAVE complex, and actin filaments, highlighting ACTR3C??s integrative role.
Disruption of ACTR3C in HeLa cells provides a physiologically relevant model to dissect how actin dynamics contribute to cancer cell behavior. Given the host cell??s p53/Rb deficiency and transformed phenotype, ACTR3C knockout may impair actin-dependent processes such as cell migration, invasion, and nuclear organization, all of which are implicated in metastasis. This model allows direct assessment of ACTR3C??s dual roles in cytoskeletal remodeling and nuclear actin functions, shedding light on its potential as a therapeutic target.
This polyclonal ACTR3C knockout model is suitable for a variety of experimental applications, including immunofluorescence staining of the actin cytoskeleton, Boyden chamber migration and invasion assays, chromatin immunoprecipitation (ChIP) to map actin-genome interactions, and cell cycle or apoptosis profiling. Its use extends to drug screening campaigns aimed at identifying compounds that modulate actin-related pathways in cancer. For technical inquiries or custom engineering services, please contact Ascent Research.
