The GPR107 Knouckout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from HT29 colorectal adenocarcinoma cells, offering targeted disruption of the GPR107 gene. This loss?of?function model enables detailed functional studies in a cancer?relevant epithelial background. The polyclonal format avoids clonal selection artifacts, ensuring a representative knockout phenotype for robust experimental outcomes.
The HT29 cell line, originally isolated from a 44?year?old female patient, serves as a widely used model of intestinal epithelial biology. HT29 cells form polarized monolayers, exhibit differentiation capabilities, and express drug transporters, making them valuable for studying drug absorption, barrier function, and colorectal cancer pathogenesis. Their tumorigenic nature provides a relevant context for investigating organelle homeostasis in malignancy.
GPR107 is an orphan GPCR localized to the Golgi and lysosomes, where it regulates lysosomal acidification and autophagic flux. Functioning downstream of mTORC1 signaling and the transcription factor TFEB, GPR107 maintains lysosomal hydrolase activity; its knockout impairs acidification, causing accumulation of autophagic substrates such as LC3?II and p62/SQSTM1. The receptor interacts with LAMP1 and LAMP2, reinforcing its role in endolysosomal trafficking and lysosome integrity.
In HT29 colorectal adenocarcinoma cells, loss of GPR107 provides a valuable tool to study the interplay between lysosomal dysfunction and cancer biology. Colorectal tumors often rely on autophagy for survival under metabolic stress and for drug resistance. This knockout model permits dissection of how impaired lysosomal acidification affects proliferation, nutrient handling, and response to lysosomotropic agents, thus advancing understanding of lysosomal targets in colorectal cancer.
These polyclonal knockout cells are ideally suited for diverse research applications, including investigation of lysosomal biology and autophagy regulation, functional genomics screens, and drug sensitivity assays. Researchers can employ Western blotting for LC3 and p62 to monitor autophagic flux, immunofluorescence detection of LAMP1 and LC3 puncta, lysosomal pH measurement, and flow cytometry-based assessment of autophagy. The model also supports cell viability studies under nutrient deprivation, drug sensitivity profiling, and use as a CRISPR knockout control for colorectal cancer drug screening. For additional technical details or to request a quote, please contact Ascent Research.
