The FAM160B2 Knockout HCT 116 Cell Line is a precisely engineered CRISPR/Cas9-edited knockout cell line that disrupts expression of the FAM160B2 gene. This model provides a robust loss-of-function platform for studying the functional roles of FAM160B2 in human colorectal cancer cells. The knockout introduces a targeted gene disruption, resulting in the elimination of functional FAM160B2 protein, thereby enabling researchers to investigate its contributions to intracellular trafficking and signaling processes without background interference from endogenous expression.
The HCT 116 parental cell line is a widely utilized human colorectal adenocarcinoma model derived from an epithelial tumor. It exhibits microsatellite instability (MSI-high) and harbors oncogenic mutations in KRAS (G13D) and PIK3CA, rendering it highly relevant for dissecting signaling networks in colorectal cancer. These characteristics make HCT 116 an ideal host for studying processes linked to tumor progression, such as endocytosis, vesicle trafficking, and cell migration, in a genetic background that mirrors key aspects of human disease.
FAM160B2 encodes a protein containing a DENN (differentially expressed in normal and neoplastic cells) domain, which is characteristic of guanine nucleotide exchange factors (GEFs) for Rab GTPases. Accordingly, FAM160B2 is predicted to activate Rab family members such as Rab35 and Rab5 by catalyzing the exchange of GDP for GTP. Activated Rab proteins subsequently recruit specific Rab effector proteins to coordinate vesicle formation, tethering, and fusion, thus modulating endosomal dynamics and trafficking. Through this mechanism, FAM160B2 is positioned within endocytic and Rab signaling pathways, influencing the intracellular sorting and recycling of receptors and other cargo.
In the context of HCT 116 cells, FAM160B2 knockout provides a powerful tool to explore how DENN domain-mediated regulation of Rab GTPases affects colorectal cancer cell biology. Given that HCT 116 cells carry activating mutations in KRAS and PIK3CA, this model permits investigation of potential crosstalk between FAM160B2-controlled trafficking and oncogenic signaling pathways. Disruption of FAM160B2 may alter endosomal compartmentalization, thereby impacting receptor tyrosine kinase signaling, cell adhesion, and migratory properties, all of which are critical determinants of tumor aggressiveness.
Research applications of this knockout cell line include functional analyses of Rab-mediated trafficking, investigation of DENN domain proteins in cancer, and assessment of phenotypic changes in migration and invasion using assays such as wound-healing and Transwell tests. The model is compatible with standard molecular and cellular techniques, including Western blotting, RT-qPCR, immunofluorescence, and endocytosis assays with fluorescent ligands. These approaches enable systematic dissection of FAM160B2??s role in endosomal pathways and its contribution to colorectal cancer progression. For additional technical specifications and ordering information, please contact Ascent Research.
