The GOLPH3L Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disrupted GOLPH3L, providing a loss-of-function model for studying Golgi biology and epithelial cancer signaling. The polyclonal format ensures robust population-level analyses without clonal artifacts. Derived from the HT29 colorectal adenocarcinoma cell line, these cells are suited for advanced research into vesicular trafficking and tumor behavior.
The HT29 cell line is a widely used epithelial model derived from human colorectal adenocarcinoma, employed to study intestinal biology, colorectal cancer, and secretory pathway regulation. Its well-characterized background and stable growth properties make it an ideal host for CRISPR-mediated gene disruption, enabling dissection of Golgi-dependent processes in a disease-relevant context.
GOLPH3L is a Golgi-localized protein that binds phosphatidylinositol 4-phosphate (PI4P) to regulate organelle morphology and vesicular trafficking. Acting downstream of PI4P levels, Golgi stress, and PKD family kinases, GOLPH3L interacts with GOLGA2, MYO18A, the coatomer complex, and ARF1 to coordinate vesicle budding and cargo transport. By modulating protein secretion and surface receptor delivery, it influences glycosylation, cell adhesion, migration, and proliferation. Disruption of GOLPH3L can impair PI4P-dependent trafficking pathways, with significant implications for Golgi structure and cellular signaling.
Loss of GOLPH3L in the HT29 colorectal adenocarcinoma background enables dissection of Golgi trafficking??s role in epithelial tumorigenesis. Aberrant Golgi structure and secretion are hallmarks of colorectal cancer, linked to invasion and drug resistance. This knockout model allows systematic analysis of GOLPH3L-dependent PI4P signaling and MYO18A-mediated Golgi dynamics on cell surface receptor profiles, signal transduction, and metabolism, offering a relevant platform for Golgi-targeted therapeutic studies and colorectal cancer vulnerability assessment.
Applications include immunofluorescence for Golgi morphology, transwell and wound-healing assays for migration and invasion, and flow cytometry for surface receptor profiling. Co-immunoprecipitation and phospho-signaling studies enable mapping of GOLPH3L interactions and downstream pathways, complemented by RNA-seq and metabolic assays to assess global changes. These applications facilitate mechanistic studies, drug sensitivity testing, and functional genomics screens. For further information, please contact Ascent Research.
