The IFI27 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the human IFI27 gene within the A2780 ovarian carcinoma cell line. This loss-of-function model was generated using the CRISPR/Cas9 system to introduce targeted gene disruption in a bulk population, yielding a heterogeneous pool of edited cells that collectively lack functional IFI27 expression. As a polyclonal product, it avoids the clonal selection artifacts often associated with single-cell-derived knockouts, providing a more diverse genetic background that is representative of the original tumor cell population. The resulting polyclonal knockout cells serve as a robust and versatile tool for dissecting IFI27-dependent biological processes in a cancer-relevant setting.
The A2780 cell line is a well-established human ovarian endometrioid adenocarcinoma model derived from an untreated patient, serving as a widely used epithelial ovarian cancer model in biomedical research. It retains key characteristics of ovarian carcinoma, including epithelial morphology and relevant oncogenic signaling alterations, making it an ideal host for studying gene function in the context of ovarian cancer. The A2780 line is particularly valued for its utility in investigating mechanisms of chemoresistance, apoptosis regulation, and hormone responsiveness, all of which are critical areas in ovarian cancer biology. By engineering the IFI27 knockout in this endogenous tumor model, researchers can directly assess the gene??s contribution to ovarian cancer cell behavior under physiologically relevant conditions.
IFI27 is an interferon-stimulated gene that encodes a mitochondrial protein critically involved in promoting intrinsic apoptosis. Its expression is robustly induced by type I interferons (IFN-?? and IFN-??) through the JAK-STAT signaling cascade, involving activation of upstream kinases JAK1 and TYK2, phosphorylation of STAT1 and STAT2, and their assembly with IRF9 to form the ISGF3 complex, which binds to interferon-stimulated response elements (ISRE) in the IFI27 promoter. Additional transcriptional regulators such as IRF1, IRF3, and IRF7 also contribute to IFI27 induction. At the protein level, IFI27 localizes to mitochondria where it interacts with Bcl-2 family members, including the anti-apoptotic Bcl-2 and pro-apoptotic Bax. Through these interactions, IFI27 facilitates mitochondrial outer membrane permeabilization, resulting in the release of cytochrome c into the cytosol. Cytochrome c then associates with Apaf-1 to form the apoptosome, which activates initiator caspase-9 and subsequently effector caspase-3, executing the apoptotic program. Furthermore, IFI27 interacts with N-myc interactor (NMI), a modulator of STAT-mediated transcription, suggesting additional regulatory crosstalk within interferon signaling networks.
In the context of the A2780 epithelial ovarian cancer model, disruption of IFI27 expression is expected to significantly attenuate interferon-induced mitochondrial apoptosis and may alter cellular responses to cytokine stress, chemotherapeutic agents, and viral infection. Given the critical role of apoptosis evasion in tumor progression and drug resistance, this knockout model provides a relevant system to dissect IFI27??s contribution to ovarian carcinoma cell survival. Loss of IFI27 function may reveal compensatory or alternative death pathways and help elucidate mechanisms underlying resistance to therapies that rely on apoptotic induction. Moreover, because IFI27 is implicated in antiviral defense via interferon signaling, these cells allow investigation of how mitochondrial apoptosis intersects with innate immune responses in cancer cells, potentially identifying new targets for combination therapies.
Researchers can employ this polyclonal knockout cell population to address key questions in cancer cell death mechanisms, interferon biology, and therapeutic resistance. Representative applications include assessing interferon-induced apoptosis using Annexin V/PI staining or TUNEL assays, monitoring mitochondrial membrane potential changes, and quantifying expression of IFI27 and downstream effectors (Bcl-2, Bax, cleaved caspase-3) by Western blotting and RT-qPCR. The model is also suitable for antiviral signaling studies, evaluating interferon-stimulated gene (ISG) induction, and testing ovarian cancer drug resistance in viability assays. Knockout confirmation can be performed by Sanger sequencing of the target locus and flow cytometry-based apoptosis profiling. For further information on this product, please contact Ascent Research.
