The IFI27 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the IFI27 gene has been disrupted to eliminate its expression. This loss-of-function model enables robust functional studies in a human cervical epithelial carcinoma background. As a polyclonal population, the cells collectively harbor various gene-editing events, providing a versatile tool for investigating interferon-induced processes without clonal biases.
The parental Ca Ski cell line is an HPV-16 positive cervical carcinoma-derived adherent line from a 40-year-old female metastasis. These tumorigenic cells serve as a classical model for HPV-driven cervical cancer, expressing viral oncoproteins E6 and E7 that disrupt tumor suppressors p53 and pRb. This background facilitates exploration of host-virus interactions and apoptosis regulation.
IFI27 is an interferon-stimulated gene that encodes a mitochondrial protein crucial for intrinsic apoptosis. Its transcription is induced by IFN-alpha/beta through JAK1/TYK2 kinase activation, leading to phosphorylation of STAT1/STAT2, which complex with IRF9 to bind ISREs in the IFI27 promoter. Once expressed, IFI27 localizes to mitochondria and interacts with VDAC and Bcl-2 family members, promoting membrane permeabilization, cytochrome c release, and activation of caspase-3 via BAX/BAK. Thus, IFI27 directly couples interferon signaling to mitochondrial apoptotic machinery.
In Ca Ski cells, IFI27 knockout abrogates interferon-induced apoptosis, unmasking the interplay between antiviral signaling, mitochondrial regulation, and HPV-mediated survival. Since HPV E6/E7 inhibit apoptosis, loss of IFI27 may shift cells toward a more survival-prone phenotype, allowing dissection of compensatory pathways. This system is valuable for studying how HPV manipulates interferon responses to evade immune destruction during cervical carcinogenesis.
Applications include IFN-alpha treatment time courses coupled with RT-qPCR for ISG profiling, western blotting for IFI27 and cleaved caspase-3, and flow cytometry for Annexin V/PI and JC-1 mitochondrial potential assays. MTT viability and HPV E6/E7 expression analysis further support antiviral drug screening and mechanistic studies. For technical support, contact Ascent Research.
