The CD63 Knockout 769-P Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population from the 769-P human renal cell carcinoma line, featuring disruption of the CD63 gene. This polyclonal pool enables studies of tetraspanin biology without clonal selection bias, serving as a versatile tool for investigating CD63 roles in exosome biogenesis, adhesion, and migration in a renal carcinoma context.
The 769-P cell line is an adherent, epithelial model derived from a primary clear cell adenocarcinoma of the kidney (ATCC CRL-1933). It recapitulates clear cell renal cell carcinoma (ccRCC) features, including hypoxia signaling and metabolic alterations, making it relevant for studying cancer cell behavior, drug sensitivity, and metastasis.
CD63, a tetraspanin family member, organizes tetraspanin-enriched microdomains that coordinate cell adhesion, migration, and endosomal trafficking. It regulates exosome biogenesis and integrin recycling, interacting directly with ITGB1, CD9, CD81, and syntenin-1. Upstream inputs include integrin activation, MITF, TGF-??, and hypoxia; downstream it modulates PI3K/AKT and ERK1/2 signaling, exosome secretion, and migratory machinery. CD63 also associates with CXCR4, EWI-2, TIMP-1, and Rab GTPases, positioning it as a key node in membrane organization and signal transduction.
In 769-P cells, CD63 knockout disrupts microdomain integrity, impairing integrin trafficking and exosome output. This leads to attenuated PI3K/AKT and ERK activation, reducing migration and invasion??critical processes in ccRCC metastasis. CD63 loss may also influence drug resistance and tumor microenvironment communication by altering exosomal cargo transfer, offering a system to dissect tetraspanin-dependent contributions to renal carcinoma aggressiveness.
Applications include exosome biogenesis studies via NTA and Western blotting, cell migration/invasion assays, integrin trafficking analysis by flow cytometry and immunofluorescence, co-IP for CD63 complexes, RT-qPCR for gene expression, and phospho-signaling analysis. The cells support research into tumor microenvironment interactions, hypoxia responsiveness, and targeted therapy resistance. For further details, contact Ascent Research.
