The HCFC1R1 Knockout KYSE-150 Polyclonal Cells product consists of a genetically heterogeneous population of KYSE-150 esophageal squamous cell carcinoma cells harboring CRISPR/Cas9-mediated disruption of the HCFC1R1 gene. This polyclonal knockout format maintains cellular diversity, offering a physiologically relevant loss-of-function model that avoids the clonal artifacts associated with single-cell-derived lines. By preserving the inherent heterogeneity of the tumor microenvironment, these polyclonal knockout cells enable robust functional studies and high-content screening applications.
The KYSE-150 parental cell line was established from a poorly differentiated esophageal squamous cell carcinoma resected from a Japanese patient and has become a widely used in vitro model for ESCC. Characterized by aggressive proliferation and compromised apoptotic signaling, KYSE-150 cells recapitulate key aspects of esophageal oncogenesis, partly driven by aberrant E2F transcriptional activity. The introduction of a targeted gene knockout into this well-characterized background generates a powerful platform for dissecting HCFC1R1 function in a disease-relevant context.
HCFC1R1 functions as a negative regulator of HCFC1 by recruiting the SIN3A/HDAC corepressor complex to repress E2F target genes. Normally, it suppresses cyclin A, cyclin E, and CDK2, restraining G1/S transition, while also modulating Bcl-2 and Bax. Knockout relieves repression, enhancing HCFC1-mediated transactivation of E2F1-3 downstream of RB1. This integrates cell cycle and DNA damage signals via p53, positioning HCFC1R1 at the interface of proliferation and apoptosis.
In the KYSE-150 ESCC model, knockout of HCFC1R1 is predicted to enhance HCFC1-dependent transactivation of E2F targets, fostering cell cycle progression and apoptosis resistance. This polyclonal knockout population enables dissection of the RB-E2F axis, DNA damage checkpoint integrity, and the interplay between pro-survival and pro-death signals in a poorly differentiated carcinoma background. Consequently, it serves as a valuable tool for identifying molecular dependencies and testing therapeutic interventions aimed at restoring cell cycle control or inducing apoptosis in esophageal cancer.
Applications include functional genomics, cell cycle and apoptosis studies, and drug target validation. Assays: western blotting (HCFC1R1, HCFC1), RT-qPCR (E2F targets), propidium iodide flow cytometry, Annexin V/PI apoptosis assay, MTS proliferation assay, RNA-seq, and co-IP of HCFC1-HCFC1R1. For inquiries, contact Ascent Research.
