The IFT88 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population originating from the 143B human osteosarcoma cell line, in which the IFT88 gene has been disrupted to eliminate functional IFT88 protein expression. This polyclonal format encompasses a diverse array of editing events, ensuring a stable, heterogeneous model that minimizes clonal selection bias while enabling robust loss-of-function analyses of primary cilium biology.
The 143B parental line is a thymidine kinase (TK)-negative derivative of the HOS osteosarcoma cell line, initially derived from a patient with highly invasive bone cancer. Demonstrating strong tumorigenicity and metastatic capacity in mouse xenograft models, 143B cells serve as a well-established platform for investigating bone tumor progression and metastasis. The cells maintain mesenchymal morphology and possess primary cilia, making them an appropriate host for studying the functional consequences of IFT88 loss on cilia-dependent processes.
IFT88 is a core component of the IFT-B complex, essential for anterograde transport of ciliary precursors via kinesin-2 motors. It interacts with IFT20, IFT52, IFT57, IFT74, and IFT81 to assemble functional IFT-B particles. Transcription of IFT88 is activated by RFX3 and FoxJ1, while downstream targets include the Hedgehog transcription factors GLI1 and GLI2, the cell cycle regulator CCND1, and the receptor tyrosine kinase PDGFR??. IFT88 ablation blocks primary cilium biogenesis, thereby disrupting Hedgehog signaling through the Patched/Smoothened/GLI axis and attenuating PDGFR?? and Wnt pathways.
In this 143B context, IFT88 knockout ablates primary cilium assembly and creates a powerful experimental tool for elucidating how ciliary signaling controls osteosarcoma aggressiveness. The model is particularly valuable for dissecting the contribution of Hedgehog pathway activity, mediated by GLI transcription factors, to cell migration and invasion in a metastatic bone cancer setting. Additionally, it facilitates investigation of PDGFR??-dependent chemotactic responses and Wnt pathway modulation downstream of ciliary dysfunction.
Applications of the IFT88 Knockout 143B Polyclonal Cells include ciliopathy disease modeling, functional studies of primary cilia in bone metastasis, and screening of small-molecule Hedgehog pathway inhibitors. Representative assays include immunofluorescence detection of ciliary markers acetylated ??-tubulin and ARL13B, western blot confirmation of IFT88 deficiency, RT-qPCR measurement of GLI1 and CCND1 transcript levels, transwell migration and invasion assays, MTT-based cell viability assessment, and flow cytometry for cell cycle distribution. For detailed product specifications, batch-specific knockout validation data, and technical support, please contact Ascent Research.
