The ALPP Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Ca Ski human cervical carcinoma cells engineered for loss-of-function studies of the ALPP gene. This product contains a heterogeneous mix of edited cells without single-cell cloning, providing a biologically diverse model for investigating ALPP-deficient phenotypes. By maintaining the polyclonal background, it avoids clonal artifacts and offers a cost-effective means to interrogate gene function in a disease-relevant setting.
Ca Ski is an epithelial cell line derived from a cervical epidermoid carcinoma metastasis that harbors integrated HPV-16 genomes. Widely adopted as a model for HPV-positive cervical cancer, these cells express viral oncogenes E6 and E7, which compromise p53 and retinoblastoma protein functions. Their transformed phenotype includes anchorage-independent growth and tumorigenicity, making them a well-characterized platform for studying molecular mechanisms of cervical carcinogenesis. This background is particularly suited to assess the contribution of ALPP in HPV-driven malignancy.
The ALPP gene encodes placental alkaline phosphatase, a GPI-anchored ectoenzyme that hydrolyzes phosphate monoesters, generating adenosine and regulating extracellular phosphate. Its expression is controlled by transcription factors including SP1 and GATA proteins, and by retinoic acid signaling. ALPP localizes to lipid rafts, interacts with GPI-anchor synthesis machinery, and forms homodimers essential for activity. Downstream, adenosine acts on purinergic receptors (A1, A2A, A2B) to modulate cellular processes such as proliferation and immune responses. Consequently, ALPP knockout in Ca Ski cells disrupts phosphate homeostasis and adenosine production, potentially altering purinergic signaling and tumor cell behavior. By eliminating ALPP activity, researchers can dissect its role in these interconnected metabolic and signaling networks.
In cervical cancer, ALPP is often elevated and has been investigated as a tumor marker, though its functional role remains unclear. The knockout model in Ca Ski cells allows direct examination of how ALPP loss affects tumorigenic properties such as proliferation, migration, and invasion in the context of HPV-16 oncogene expression. Moreover, it enables exploration of crosstalk between ALPP-mediated adenosine signaling and HPV-driven pathways. Because Ca Ski cells represent an invasive and metastatic phenotype, this system is valuable for studying ALPP??s contributions to advanced disease states.
This polyclonal knockout cell population supports diverse applications including functional assays (proliferation, migration/invasion), alkaline phosphatase activity measurements, HPLC-based adenosine quantification, and phospho-signaling analysis. It is suitable for inhibitor screening targeting alkaline phosphatases or purinergic receptors, as well as for RNA-seq and flow cytometric characterization. The product provides a flexible tool for researchers investigating phosphate metabolism, purinergic signaling, and cervical cancer biology. For additional information or technical support, please contact Ascent Research.
