EHD3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HeLa cell line, engineered for disruption of the EHD3 gene. This polyclonal knockout model enables loss-of-function studies of EHD3 without clonal selection, providing a heterogeneous population that reflects the genetic diversity of edited cells. The cells are ideal for investigating EHD3-dependent processes in human cervical adenocarcinoma.
The parental HeLa cell line, isolated from a cervical adenocarcinoma of Henrietta Lacks, is HPV18-positive and immortalized, serving as a widely used model for cancer and cell biology research. These epithelial cells retain key characteristics of cervical carcinoma and are permissive to a broad range of experimental manipulations, making them suitable for endocytic trafficking and cell migration studies.
EHD3 encodes an ATP-dependent membrane remodeling ATPase that orchestrates endocytic recycling of receptors, including the transferrin receptor and EGFR, to control their surface expression and downstream signaling. Acting downstream of EGF stimulation and HIF-1?? transcriptional programs, and regulated by miR-125b, EHD3 interacts with the EHD1/EHD2 family, Rab11, Arp2/3 complex, and myosin to facilitate receptor trafficking back to the plasma membrane. Through these interactions, EHD3 modulates recycling of integrins and other cargos, thereby influencing actin cytoskeletal dynamics, cell migration, and proliferation. Loss of EHD3 disrupts this recycling network, leading to altered receptor distribution and attenuated signaling.
In the HeLa cervical adenocarcinoma context, EHD3 knockout is particularly relevant given its role in EGFR trafficking and cell migration??processes often dysregulated in HPV-driven cancers. EHD3 has also been implicated in breast cancer and glioblastoma, extending the utility of this model beyond cervical carcinoma. Disruption of EHD3 in these cells can reveal dependencies on endocytic recycling for tumor cell motility and invasive behavior, and may uncover therapeutic vulnerabilities.
This polyclonal knockout cell population is suited for a variety of experimental approaches in cancer biology and cell signaling. Researchers can employ Western blotting to confirm EHD3 loss, immunofluorescence to assess endosomal marker distribution, and flow cytometry to measure transferrin uptake as a functional readout of receptor recycling. Functional assays such as wound healing and Transwell migration can directly probe the impact of EHD3 disruption on cell motility, while EGFR phosphorylation analysis can link trafficking defects to signaling outcomes. These cells also support drug resistance studies, enabling investigation of how endocytic recycling influences therapeutic response. For further details or custom configurations, please contact Ascent Research.
