In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The AKR1C3 Knockout A549 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human A549 lung adenocarcinoma cells. It provides a loss-of-function model to study AKR1C3, an aldo-keto reductase that catalyzes NADPH-dependent reduction of prostaglandin D2 and androgen precursors, disrupting PPAR?? and androgen receptor signaling. This model enables investigation of hormone and prostaglandin metabolism in alveolar type II epithelial cells. Applications include cancer biology, hormone signaling, drug metabolism, and inflammation research, with representative assays such as western blotting, RT-qPCR, proliferation and migration assays, and metabolite quantification. The cell line is a valuable resource for dissecting AKR1C3-dependent pathways and for drug screening in lung cancer studies.
CALHM2 Knockout 786O Polyclonal Cells
Cat. No. ARG35717
CSDE1 Knockout SKOV3 Polyclonal Cells
Cat. No. ARG12414
MTFR1L Knockout Hela Polyclonal Cells
Cat. No. ARG8853
MSN Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17873
ETS1 Knockout 786-O Polyclonal Cells
Cat. No. ARG5253
GLYR1 Knockout AGS Polyclonal Cells
Cat. No. ARG2616
The AKR1C3 Knockout A549 Cell Line is a CRISPR/Cas9-edited knockout cell line in which the AKR1C3 gene has been disrupted via CRISPR/Cas9-mediated gene targeting. This engineered loss-of-function model is derived from the A549 lung adenocarcinoma cell line and provides a defined genetic background for studying AKR1C3-dependent pathways in human alveolar type II cells. The knockout cell line enables investigation of AKR1C3’s enzymatic functions without interference from residual gene expression.
The parental A549 cell line was originally isolated from a 58-year-old Caucasian male with lung carcinoma and serves as a widely used in vitro model for alveolar type II epithelial cells. These adherent epithelial cells retain features relevant to lung adenocarcinoma biology, including expression of pathways involved in proliferation, hormone metabolism, and inflammatory responses. The A549 background is well-characterized and suitable for functional genomics studies in cancer and metabolic research.
AKR1C3 encodes an aldo-keto reductase that catalyzes NADPH-dependent reduction of carbonyl substrates, central to steroid hormone and prostaglandin metabolism. The enzyme acts downstream of glucocorticoid receptor (NR3C1) and androgen receptor (AR) and is regulated by IL-6/STAT3 signaling and oxidative stress via NFE2L2. AKR1C3 converts prostaglandin D2 to 9??,11??-prostaglandin F2, which attenuates PPAR?? activity, and reduces androgen precursors to active androgens such as testosterone and dihydrotestosterone, promoting AR-mediated transcription. Disruption of AKR1C3 abrogates these conversions, impacting PPAR?? and AR signaling networks.
In the A549 background, AKR1C3 knockout eliminates reduction of prostaglandin D2 and androgen precursors, leading to accumulation of prostaglandin D2 and diminished androgen receptor signaling. This disruption modulates cell proliferation, migration, and inflammatory responses, reflecting the gene’s involvement in lung cancer progression and hormone-dependent pathways. The knockout thus provides a precise model to investigate AKR1C3-mediated contributions to tumor biology and signaling cross-talk in lung epithelial cells.
This knockout cell line enables a broad range of research applications, including cancer biology, hormone signaling, drug metabolism, and inflammation. Representative assays include western blotting, RT-qPCR, cell proliferation and migration assays, androgen/prostaglandin metabolite quantification, and drug sensitivity screening. It is particularly valuable for mechanistic studies of AKR1C3 in lung adenocarcinoma and for screening inhibitors targeting aldo-keto reductase pathways. For inquiries, please contact Ascent Research.
