The C11orf68 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line. This loss-of-function model targets the C11orf68 gene, which encodes a mitochondrial protein involved in cell proliferation and apoptosis. The polyclonal format maintains genetic heterogeneity while ensuring efficient target-gene disruption, providing a robust tool for investigating hepatocellular carcinoma biology and mitochondrial signaling.
SK-HEP-1 cells were originally isolated from the ascites of a male patient with liver adenocarcinoma and display an epithelial morphology. As a well-established model for hepatocellular carcinoma, this cell line endogenously expresses key components of the PI3K/AKT pathway, making it advantageous for studying mitochondrial regulation of tumor cell viability and apoptosis. The SK-HEP-1 background supports mechanistic studies and drug-screening applications relevant to liver cancer.
C11orf68 operates at the intersection of mitochondrial function and AKT-mediated survival signaling. Its expression is driven by upstream transcription factors MYC and E2F1. Functionally, C11orf68 promotes cell proliferation and inhibits apoptosis by sustaining AKT1 phosphorylation. It physically interacts with anti-apoptotic BCL2L1 and pro-apoptotic BAX, and its disruption leads to reduced AKT signaling, activation of CASP9, and initiation of the intrinsic apoptosis cascade. Downstream effectors include BCL2 family members, cyclins, and CDKs, linking the gene to cell cycle and death machinery.
Knockout of C11orf68 in SK-HEP-1 cells creates a disease-relevant model for dissecting mitochondrial contributions to hepatocellular carcinoma pathogenesis. Loss of this protein attenuates survival signals through AKT1 and MTOR while releasing the apoptotic constraints governed by BCL2/BAX dynamics. This system enables precise examination of mitochondrial perturbation effects on tumor cell fate and therapy resistance, avoiding clonal artifacts common in single-cell-derived lines.
This knockout model is suited for studying C11orf68-dependent tumor progression, screening compounds that modulate mitochondrial apoptosis pathways, and validating therapeutic targets within the PI3K/AKT/BCL2 axis. Representative assays include western blotting for phospho-AKT, flow cytometry with Annexin V/PI staining, MTT or CCK-8 proliferation assays, JC-1 mitochondrial membrane potential measurements, and RT-qPCR for downstream transcriptional targets. For further details or custom inquiries, please contact Ascent Research.
