The CCDC102A Knockout NCI-H1975 Polyclonal Cells product provides a polyclonal population of NCI-H1975 cells with CRISPR/Cas9-mediated disruption of the CCDC102A gene. This product is designed as a loss-of-function model to investigate the role of CCDC102A in cell migration, invasion, and associated signaling networks. The polyclonal format preserves genetic heterogeneity and reflects the complexity of a knockout pool, enabling robust and reproducible phenotypic analyses without clonal artifacts. This gene-edited cell product is suitable for studying CCDC102A function in a non-small cell lung cancer context.
The parental NCI-H1975 cell line is a widely used human lung adenocarcinoma model derived from non-small cell lung cancer. These epithelial cells harbor an activating EGFR exon 19 deletion (E746-A750del) and a p53 mutation, while KRAS remains wild-type. This genetic background drives intrinsic oncogenic signaling and provides a clinically relevant system for investigating tumor progression and therapeutic resistance. NCI-H1975 cells exhibit properties characteristic of aggressive lung adenocarcinoma, including invasive potential and responsiveness to EGFR-targeted agents.
CCDC102A encodes a coiled-coil domain protein implicated in promoting cell migration and invasion through regulation of cytoskeletal dynamics. Mechanistically, CCDC102A functions downstream of TGF-?? signaling and the transcription factors SNAI1 and TWIST1, key drivers of epithelial-mesenchymal transition (EMT). It modulates actin polymerization and focal adhesion turnover, likely through interactions with Rho GTPases and actin-binding proteins. CCDC102A additionally forms heterodimers with CCDC102B and influences the expression of matrix metalloproteinases MMP2 and MMP9. Loss of CCDC102A disrupts these processes, offering insight into pathways governing E-cadherin to N-cadherin switching, vimentin upregulation, and integrin-FAK-paxillin signaling during EMT.
In NCI-H1975 cells, CCDC102A knockout models the attenuation of metastatic drivers in a lung adenocarcinoma background with defined oncogenic mutations. The EGFR and p53 alterations synergize with EMT-regulating networks, making this system particularly relevant for dissecting CCDC102A-dependent invasion mechanisms. This knockout model empowers detailed investigation of how cytoskeletal reorganization and focal adhesion dynamics contribute to the metastatic cascade in non-small cell lung cancer, potentially revealing vulnerabilities for therapeutic intervention.
This product is ideally suited for functional assays such as wound healing and transwell invasion to quantify migratory and invasive capacity. Researchers can monitor EMT marker profiles by Western blotting for E-cadherin, N-cadherin, and vimentin, or visualize actin cytoskeletal architecture via immunofluorescence. Co-immunoprecipitation studies can validate CCDC102A protein interactions, while RT-qPCR allows transcript-level analysis of MMP2, MMP9, and Rho GTPase targets. These applications position the CCDC102A Knockout NCI-H1975 Polyclonal Cells as a versatile tool for metastatic cancer research and anti-metastatic drug screening. For further information, please contact Ascent Research.
