The AKR1C2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the near-haploid HAP1 cell line, featuring targeted disruption of the AKR1C2 gene. This pool of heterogeneously edited cells enables robust loss-of-function studies without clonal selection artefacts. The polyclonal format is ideally suited for experiments requiring population-level readouts, such as pooled screening or metabolic profiling, providing a convenient knockout model for aldo-keto reductase family 1 member C2 research.
HAP1 is a suspension-adapted human cell line originally derived from the chronic myeloid leukemia KBM-7 line. Its near-haploid karyotype means that disruption of a single allele typically yields a functional null phenotype, making it a powerful host for genetic knockout studies. Widely adopted for functional genomics, HAP1 combines ease of culture with high editing efficiency and compatibility with various high-throughput screening platforms.
AKR1C2 encodes an NADPH-dependent aldo-keto reductase that catalyzes the reduction of ketosteroids and steroid hormones, converting progesterone to 20??-hydroxyprogesterone and dihydrotestosterone to 3??-androstanediol, thus attenuating androgen and progesterone receptor signaling. Its transcription is regulated by FOXA1, the androgen receptor, interleukin-1??, and glucocorticoids. The enzyme functionally interacts with the related isoforms AKR1C1 and AKR1C3 and operates downstream of the steroid 5??-reductases SRD5A1 and SRD5A2 and upstream of HSD17B6 within steroidogenic pathways. These interactions position AKR1C2 as a critical modulator of hormone receptor activity and steroid metabolic flux.
Disruption of AKR1C2 in the haploid HAP1 background results in a profound loss of reductase function, establishing a defined model for investigating hormone-dependent cancers such as prostate and breast cancer, as well as endometriosis and polycystic ovary syndrome. The polyclonal population captures diverse editing events, avoiding single-cell cloning bias and better reflecting the heterogeneity of tumor cell populations. This system also supports exploration of xenobiotic and bile acid metabolism, for which AKR1C2 activity is relevant.
This knockout cell pool is amenable to confirmation of gene disruption via Sanger sequencing and TIDE analysis, as well as expression analyses by RT-qPCR and western blotting. Functional assays including LC-MS-based steroid profiling and androgen or progesterone receptor luciferase reporter assays can delineate altered hormone signaling. Additional applications encompass drug sensitivity and cell viability testing for therapeutic evaluation, and the cells integrate seamlessly into functional genomic screens. For further product information or to discuss specific experimental requirements, please contact Ascent Research.
