The INO80C Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited heterogeneous population of A-549 human lung adenocarcinoma epithelial cells with targeted disruption of the INO80C gene. This loss-of-function model avoids clonal selection, preserving polyclonal diversity that mirrors physiological knockout scenarios. The polyclonal format is suitable for studying gene function without confounding clonal artifacts, enabling robust analysis of INO80C-dependent cellular processes.
Derived from a 58-year-old Caucasian male, the parental A-549 cell line is a cornerstone model for non-small cell lung cancer research. These adherent epithelial cells harbor an activating KRAS mutation and wild-type p53, capturing critical oncogenic and tumor-suppressive pathways. Their extensive characterization in drug resistance, signaling, and epithelial biology provides a well-defined context for interrogating chromatin remodeling in lung adenocarcinoma.
INO80C is an integral subunit of the multi-protein INO80 chromatin remodeling complex, which includes INO80, INO80B, ACTR5, ACTR8, IES2, IES6, UCH37, NFRKB, and MCRS1. This ATP-dependent remodeler orchestrates nucleosome sliding and histone exchange to regulate transcription, DNA replication, and double-strand break repair. Upstream, INO80C activity is responsive to DNA damage signals mediated by ATM and ATR kinases. Downstream, the complex targets nucleosome occupancy at specific genomic loci, controlling gene expression programs and preserving genome integrity.
Knocking out INO80C in A-549 cells dismantles the INO80 complex, compromising chromatin-mediated DNA repair and transcriptional regulation. This disruption heightens genomic instability, sensitizes cells to genotoxic stress, and may alter oncogenic transcription networks. The model is thus instrumental for deciphering how chromatin remodelers sustain lung cancer cell survival and for probing vulnerabilities exploitable by epigenetic therapies.
Applications include validation of INO80C protein loss by western blot, transcriptome profiling via RNA-seq, ChIP-qPCR for histone modifications (e.g., H3K9ac), DNA damage assessment through ??-H2AX immunofluorescence, and functional assays such as MTT viability, Annexin V apoptosis, flow cytometric cell cycle analysis, and colony formation. These tools enable investigation of INO80C function in lung cancer chromatin biology, synthetic lethal interactions with DNA-damaging chemotherapeutics, and drug sensitivity studies targeting chromatin remodelers. For inquiries, contact Ascent Research.
