The ADTRP Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, designed to disrupt the ADTRP gene. This loss-of-function model enables researchers to investigate the functional roles of ADTRP in cellular processes such as coagulation and angiogenesis, without the constraints of monoclonal selection. The polyclonal format provides a heterogeneous knockout pool, facilitating robust downstream analyses in cancer biology and cardiovascular research. The product is generated using state-of-the-art gene editing technology to ensure efficient disruption of ADTRP, offering a versatile tool for pathway deconvolution and target validation studies.
HeLa cells, the host line, are an immortalized human cervical adenocarcinoma epithelial cell line originally isolated from Henrietta Lacks. These cells are HPV-18 positive and exhibit aggressive tumorigenic properties, making them a fundamental model for studying cancer mechanisms, signal transduction, and therapeutic responses. Their robust growth characteristics and extensive characterization across biomedical fields provide an optimal cellular background for investigating gene function in oncogenic contexts. The well-documented HeLa genome facilitates the interpretation of knockout phenotypes and integration with existing literature.
ADTRP encodes an androgen-dependent regulator of tissue factor pathway inhibitor (TFPI) expression, playing a critical role in maintaining vascular homeostasis. It transcriptionally regulates TFPI in response to androgen receptor (AR) activation by androgens such as testosterone and dihydrotestosterone (DHT). Mechanistically, ADTRP functions upstream of TFPI and modulates key signaling cascades, including PI3K/AKT and MAPK pathways, where it influences the phosphorylation of AKT and ERK1/2. This regulation coordinates downstream effectors like matrix metalloproteinases MMP2 and MMP9, impacting endothelial cell function, angiogenesis, and coagulation balance. ADTRP??s interaction with AR and TFPI underscores its position at the intersection of hormonal signaling and hemostatic control.
In the HeLa cancer model, ADTRP disruption provides a physiologically relevant platform to dissect the gene??s contributions to tumor progression and cardiovascular pathology. Given HeLa cells?? tumorigenic nature, ADTRP knockout allows for detailed examination of androgen receptor signaling in cervical cancer, as well as its involvement in cell migration and invasion through MMP2/MMP9-mediated extracellular matrix remodeling. Additionally, this model recapitulates aspects of ADTRP-associated diseases such as coronary artery disease and myocardial infarction, enabling studies that bridge oncogenic transformation and coagulation defects. The polyclonal knockout captures diverse mutational events, reducing clonal bias and enhancing the identification of robust phenotypic changes.
Researchers can employ this polyclonal knockout cell population in a variety of experimental contexts. Applications include coagulation assays to measure thrombin generation, tube formation assays to assess angiogenesis, and wound healing or transwell assays to evaluate cell migration and invasion. The model is also suitable for high-throughput drug screening targeting androgen-dependent pathways or TFPI expression, with readouts such as western blotting for ADTRP and downstream targets, RT-qPCR for mRNA quantification, and androgen receptor luciferase reporter assays. Immunofluorescence can be used to analyze ADTRP localization. For additional information, please contact Ascent Research.
