The IFT27 Knockout A-549 Polyclonal Cells are a heterogeneous population of CRISPR/Cas9-edited A-549 lung adenocarcinoma epithelial cells carrying targeted disruption of the IFT27 gene. This polyclonal knockout model provides a genetically diverse background for investigating intraflagellar transport (IFT)-dependent processes and Hedgehog signaling without the confounding effects of clonal selection. By eliminating IFT27 function, researchers can dissect ciliary assembly mechanisms and cilia-mediated signal transduction in a human cancer-derived cellular context suitable for advanced biomedical applications.
The A-549 host cell line was established from a 58-year-old male patient with lung adenocarcinoma and carries an activating KRAS G12S mutation. These cells exhibit adherent epithelial morphology and display characteristics of alveolar type II pneumocytes, making them a standard model for studies of respiratory disease and oncogenic transformation. Their robust growth and amenability to genetic manipulation support downstream functional analyses.
IFT27 encodes a small GTPase that is an essential component of the IFT-B complex, localizing to the ciliary tip and governing retrograde intraflagellar transport. It physically interacts with IFT25, IFT74, IFT81, and the BBSome. Transcription of IFT27 is regulated by ciliogenic transcription factors RFX3 and FOXJ1, and its activity is modulated by Hedgehog pathway activation and cellular stress. Genetic disruption of IFT27 compromises ciliary tip remodeling, leading to impaired processing of GLI transcription factors (GLI1, GLI2, GLI3) and diminished expression of downstream targets such as PTCH1 and SMO, collectively dampening Hedgehog signal transduction.
In the A-549 context, primary cilia and Hedgehog signaling have been implicated in tumor cell plasticity, migration, and drug resistance. IFT27 knockout in this polyclonal population abolishes efficient ciliogenesis and attenuates GLI-dependent transcriptional programs, providing a tractable system to decouple ciliary contributions from KRAS-driven oncogenic pathways. This model thus enables precise evaluation of how loss of an IFT subunit reshapes lung adenocarcinoma cell behavior.
The polyclonal IFT27 knockout cells are well-suited for ciliopathy disease modeling, Hedgehog pathway dissection, IFT complex biology studies, and drug discovery campaigns. Typical readouts include immunofluorescence staining for acetylated tubulin to assess cilia, Hedgehog-responsive luciferase reporter assays, RT-qPCR analysis of GLI target genes, and co-immunoprecipitation to interrogate protein interactions. Complementary assays such as migration/invasion scoring and RNA-seq transcriptomics broaden the investigative framework. For detailed product information, please contact Ascent Research.
