The GOLGA7 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human HT29 colorectal adenocarcinoma cell line, carrying targeted disruption of the GOLGA7 gene. This polyclonal knockout model consists of a heterogeneous mixture of gene-edited cells, which minimizes clonal selection artifacts and provides a robust background for loss-of-function experiments. The ablation of GOLGA7 protein expression allows researchers to investigate Golgi-related processes without the confounding effects of monoclonal variability.
HT29 is an epithelial cell line established from a primary colorectal adenocarcinoma. It is extensively utilized in cancer biology, drug transport, and differentiation studies due to its well-characterized growth properties and sensitivity to chemotherapeutic agents such as 5-fluorouracil. The line also exhibits enterocytic differentiation potential, offering a physiologically relevant model for studying intestinal epithelial mechanisms and colorectal tumor progression.
GOLGA7 encodes a golgin protein localized to the Golgi apparatus, where it mediates vesicle tethering, stack organization, and intra-Golgi transport. It functions downstream of ARF1 and RAB GTPases, is phosphorylated by SRC kinase, and associates with central Golgi components including GORASP2 (GRASP55), GOLGA2 (GM130), RAB2, COPI coatomer, and SNARE proteins. Mechanistically, GOLGA7 facilitates docking of transport vesicles, ensuring proper processing and secretion of glycoproteins and cell surface receptors. Its loss disrupts Golgi architecture, impairs trafficking, and reduces surface expression of targets such as EGFR.
Within HT29 cells, GOLGA7 knockout creates a relevant system for examining Golgi dysfunction in colorectal cancer. The disruption alters glycosylation patterns and receptor presentation, thereby influencing proliferation, migration, and chemosensitivity. This model enables study of how impaired trafficking modulates oncogenic signaling and drug resistance, linking Golgi pathology to clinically important phenotypes in colorectal adenocarcinoma.
The polyclonal knockout cells support diverse experimental workflows, including immunofluorescence microscopy to assess Golgi morphology, western blotting for glycoprotein maturation analysis, flow cytometry for quantifying surface EGFR levels, and ELISA-based measurement of secreted proteins. Wound healing and migration assays reveal motility defects, while drug sensitivity panels with 5-FU probe the role of Golgi-mediated processing in chemoresistance. For technical specifications or additional information, please contact Ascent Research.
