The HSD17B12 Knockout HT29 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, with targeted gene disruption of HSD17B12. This loss-of-function model facilitates investigation of the 17??-hydroxysteroid dehydrogenase 12 enzyme within an epithelial cancer context. The polyclonal format ensures representation of diverse knockout variants, minimizing biases from single-cell clonal selection and enabling robust functional analyses.
HT29 is a well-characterized colorectal adenocarcinoma cell line originally established from a 44-year-old Caucasian female. These adherent cells exhibit epithelial-like morphology and are broadly utilized in cancer research, particularly for studying tumor proliferation, metastatic potential, and drug sensitivity. The HSD17B12 knockout in HT29 provides a physiologically relevant platform to interrogate the intersection of estrogen biosynthesis and lipid metabolism in colorectal carcinogenesis.
HSD17B12 encodes a bifunctional enzyme residing in the endoplasmic reticulum that catalyzes the conversion of estrone to the more potent estrogen estradiol, thereby stimulating estrogen receptor alpha-mediated signaling. Simultaneously, HSD17B12 functions in the elongation cycle of very long-chain fatty acids, cooperating with elongases such as ELOVL1 and ELOVL3 to generate lipids critical for membrane architecture and cellular metabolism. Its expression is regulated by estradiol, androgens, PPAR??, and SREBP1. Downstream, HSD17B12 promotes estradiol accumulation and the synthesis of elongated fatty acids, modulating gene expression and lipid homeostasis. HSD17B12 cooperates with CYP19A1 and HSD17B1 in estradiol biosynthesis and with ELOVL enzymes in fatty acid elongation.
In the HT29 colorectal cancer model, disruption of HSD17B12 is predicted to diminish local estradiol production, thereby attenuating estrogen receptor signaling that may support tumor cell proliferation in estrogen-sensitive microenvironments. Concurrently, loss of HSD17B12-mediated fatty acid elongation can perturb the composition of very long-chain fatty acyl species, potentially affecting membrane fluidity, lipid raft formation, and downstream signaling pathways dependent on lipid second messengers. These dual molecular deficits create a powerful system to dissect the relative roles of steroid hormone biosynthesis and lipid metabolism in colorectal adenocarcinoma phenotypes, including cell growth, motility, and survival.
This product is ideally suited for studies of local estrogen biosynthesis in colorectal cancer, assessment of HSD17B12 as a candidate therapeutic target, and elucidation of lipid metabolic alterations in cancer cells. Experimental approaches include estradiol ELISA to measure hormone levels, fatty acid methyl ester analysis by GC-MS for lipid profiling, MTS-based proliferation assays, migration and invasion tests, RT-qPCR quantification of estrogen-responsive genes, and western blot detection of estrogen receptor alpha. For further information or to integrate HSD17B12 Knockout HT29 Polyclonal Cells into your research program, please contact Ascent Research.
