The HSD17B8 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product features a disrupted HSD17B8 gene, resulting in a loss-of-function model for investigating the roles of HSD17B8 in steroid hormone metabolism and fatty acid oxidation. The polyclonal knockout population enables gene function studies without clonal selection bias.
The HT29 cell line, originally isolated from a primary colon adenocarcinoma of a Caucasian female, is a widely utilized model for colorectal cancer research and intestinal epithelial biology. HT29 cells exhibit a capacity to differentiate into enterocyte-like cells under appropriate culture conditions, expressing markers of intestinal epithelial differentiation and producing mucus. This characteristic makes them valuable for examining tumor biology, epithelial barrier function, and metabolic adaptations in colon cancer.
HSD17B8 encodes a dual-function enzyme that catalyzes the oxidation of estradiol to estrone and testosterone to androstenedione using NAD+ as a cofactor, thereby inactivating potent sex hormones. Additionally, HSD17B8 possesses mitochondrial 3-ketoacyl-CoA thiolase activity in the final step of fatty acid ??-oxidation, contributing to acetyl-CoA generation. Upstream regulators include estrogen receptor signaling, PPAR??, and insulin signaling, while downstream targets encompass estrone, androstenedione, and modulation of estrogen receptor activity. HSD17B8 operates within a metabolic network alongside HSD17B1, HSD17B2, CYP19A1, ACAA2, and others.
Disruption of HSD17B8 in HT29 cells provides a powerful tool to dissect the interplay between steroid hormone metabolism and fatty acid oxidation in a colon cancer model. This knockout system allows researchers to investigate how loss of HSD17B8 alters hormone-dependent signaling pathways that may influence tumor growth and differentiation. The HT29 background further enables studies on metabolic reprogramming in colorectal cancer, where dysregulated fatty acid ??-oxidation and altered hormone responsiveness are implicated in disease progression.
This polyclonal knockout cell population is suitable for western blotting, RT-qPCR, enzyme activity assays with radiolabeled substrates, steroid quantification by LC-MS/MS, and fatty acid oxidation flux assays. Cell viability assays in hormone-depleted conditions can assess hormone-sensitive cancer cell survival. These cells support research on sex hormone-dependent cancers, metabolic disorders, and drug metabolism. For further details, please contact Ascent Research.
