The IGFBP5 Knockout HCT 116 Polyclonal Cells consist of a heterogeneous population of HCT 116 cells that have undergone CRISPR/Cas9-mediated disruption of the IGFBP5 gene. This polyclonal knockout pool provides a loss-of-function model for investigating the role of insulin-like growth factor-binding protein 5 (IGFBP5) in colorectal cancer biology. As a CRISPR/Cas9-edited population, the cells collectively carry a range of null mutations at the target locus, enabling robust functional studies without clonal selection artifacts. The product is designed for researchers studying IGF signaling, apoptosis, and tumor cell migration in a genetically defined background.
The HCT 116 host cell line is a well-characterized human colorectal carcinoma model exhibiting microsatellite instability (MSI-H), a KRAS G13D activating mutation, and wild-type p53 status. These features make it particularly valuable for dissecting oncogenic signaling networks and DNA damage response pathways. HCT 116 cells are widely employed in cancer research due to their reproducible growth characteristics, susceptibility to genetic manipulation, and relevance to colorectal cancer pathogenesis. The combination of mutant KRAS and intact p53 provides a unique context for examining the interplay between growth factor signaling and tumor suppression.
IGFBP5 is a multifaceted modulator of the IGF axis, binding IGF-1 and IGF-2 to limit IGF-1R activation and thereby attenuating PI3K/AKT and MAPK/ERK signaling. This leads to altered expression of downstream effectors such as AKT, ERK1/2, BCL2, BAX, and p21. Independent of IGF, IGFBP5 interacts with fibronectin, collagen, and integrins to regulate cell adhesion and migration. Its expression is controlled by p53, TGF-??, and other factors, and it in turn modulates MMPs and Smad proteins. Thus, IGFBP5 integrates growth factor, matrix, and stress signals to coordinate proliferation, apoptosis, and motility.
In HCT 116 cells, IGFBP5 knockout is predicted to enhance IGF-1R signaling, potentially increasing proliferation, survival, and invasiveness, especially given constitutive KRAS activation. With wild-type p53, IGFBP5 loss may also affect DNA damage responses and apoptosis, making this model useful for chemoresistance studies. The MSI-H background may reveal compensatory changes in other IGFBP family members. This polyclonal system thus enables dissection of IGFBP5??s dual roles as a tumor suppressor or promoter.
Key applications include colorectal cancer progression, IGF-1R/MAPK/ERK signaling analysis, apoptosis and EMT studies, and drug resistance screening. The cells are compatible with western blotting, RT-qPCR, proliferation/apoptosis assays, migration/invasion assays, co-immunoprecipitation, phospho-specific flow cytometry, and cell cycle analysis. This knockout model facilitates biomarker discovery and mechanistic studies. For further technical details, please contact Ascent Research.
