The HPSE Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with disrupted heparanase expression. This polyclonal model provides a robust loss-of-function system for investigating heparanase-mediated extracellular matrix degradation, growth factor release, and cell invasion, without requiring clonal isolation. Suitable for pooled functional assays, these cells enable studies of HPSE-dependent mechanisms relevant to cancer metastasis, angiogenesis, and inflammation.
HAP1 cells are a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia. The haploid karyotype simplifies knockout generation by requiring disruption of a single allele, enabling efficient loss-of-function studies. HAP1 retains myeloid characteristics while providing a versatile platform for functional genomics. In this HPSE knockout, the HAP1 background offers a relevant context for exploring heparanase roles in myeloid biology and leukemic signaling, complementing broader cell biology investigations.
HPSE encodes heparanase, an endoglycosidase that cleaves heparan sulfate from proteoglycans like perlecan and syndecan-1, releasing growth factors such as VEGF, FGF, and HGF. This activates MAPK/ERK, Akt/PI3K, and Wnt/??-catenin signaling, while promoting NF-??B and MMP expression. Upstream, HPSE is regulated by p53, NF-??B, HIF-1??, and growth factors including EGF. By linking ECM degradation to prometastatic pathways, HPSE controls invasive behavior and angiogenesis.
HPSE knockout in HAP1 impairs heparan sulfate degradation, reducing growth factor release and attenuating ERK, Akt, and NF-??B activation. This deficiency makes the cells highly suitable for studying heparanase-dependent invasion and migration using Matrigel and wound healing assays. The myeloid leukemia origin additionally permits investigation of heparanase contributions to leukemic cell trafficking and bone marrow niche interactions. The polyclonal nature avoids clonal artifacts, ensuring representative responses for functional and pharmacological studies.
These cells are ideal for tumor invasion, metastasis, and angiogenesis assays. Experimental approaches include zymography for heparanase activity, ELISA for growth factor release (e.g., VEGF), and co-immunoprecipitation with syndecan-1. They support drug discovery by enabling heparanase inhibitor testing and target validation in cancer and fibrosis. Inflammation models can reveal HPSE-dependent cytokine and migration effects. For additional information, please contact Ascent Research.
