Cat. No. ARG43797
The CRBN Knockout PC-3 Cell Line is a CRISPR/Cas9-edited human knockout cell line derived from PC-3 prostate adenocarcinoma cells, providing a stable loss-of-function model of cereblon. CRBN functions as the substrate receptor for the CRL4 E3 ubiquitin ligase complex, mediating degradation of targets including IKZF1 and IKZF3 in response to IMiDs. By eliminating CRBN, this line enables direct study of IMiD mechanism of action, drug resistance, and ubiquitin-proteasome regulation in an androgen-independent, metastatic prostate cancer background. It is suited for western blotting, cell viability, co-immunoprecipitation, and drug sensitivity assays, supporting research in multiple myeloma, MDS, and prostate oncology.
| Host Cell | PC-3 |
| Sex of Donor | Male |
| Age | 62 years |
| Gene Name | CRBN |
| Gene Identifier | NCBI Gene ID 51185 |
| Morphology | Epithelial-like |
| Growth Mode | Adherent |
| Storage | Liquid nitrogen (LN2) |
| Temperature | 37°C |
| Atmosphere | 5% CO₂ |
| Sterility testing | The bacterial, yeast, and fungi are not detected in these cells by daily monitor. |
| Mycoplasma testing | Negative for mycoplasma through PCR analysis |
Intended Use: This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.
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This product is provided "AS IS". For Research Use Only. Not for human or animal therapeutic use.
The CRBN Knockout PC-3 Cell Line is a human CRISPR/Cas9-edited knockout cell line with functional disruption of the CRBN gene. Derived from the PC-3 prostate adenocarcinoma cell line, this model offers a stable loss-of-function system to study cereblon (CRBN) in ubiquitin-mediated proteolysis and drug responses. The targeted disruption eliminates the substrate receptor of the CRL4-CRBN E3 ubiquitin ligase complex, providing a defined genetic background for investigating IMiD-dependent signaling and protein homeostasis.
PC-3 cells originate from a bone metastasis of grade IV prostate adenocarcinoma and serve as a widely used model of androgen-independent, castration-resistant prostate cancer. This host line lacks AR and PSA expression and exhibits strong tumorigenic and metastatic properties in vivo. The aggressive phenotype makes PC-3 cells especially suitable for dissecting pathways driving prostate cancer progression and for evaluating therapeutic vulnerabilities in a clinically relevant setting.
CRBN encodes cereblon, the substrate receptor for the CUL4-DDB1-RBX1 (CRL4) E3 ubiquitin ligase complex. CRBN binds DDB1 and CUL4A/CUL4B to form an active E3 ligase that targets endogenous substrates for proteasomal degradation. In the presence of IMiDs such as thalidomide, lenalidomide, or pomalidomide, CRBN undergoes a conformational change redirecting substrate specificity to neosubstrates including IKZF1, IKZF3, and CK1??. These are recruited, ubiquitinated, and degraded, leading to downstream effects in myeloma and other cancers. CRBN activity is further modulated by DNA damage signaling and AMPK, and interacts with E2 enzymes and targets like GSPT1 and MEIS2.
In PC-3 cells, CRBN knockout abrogates IMiD-induced degradation of neosubstrates, allowing sustained IKZF1 and IKZF3 expression. This enables direct interrogation of IMiD action and resistance in a solid tumor context, independent of endogenous CRBN. The model also dissects CRBN-dependent versus -independent functions in proliferation, migration, and metastasis. By coupling CRBN loss with the androgen-independent, metastatic features of PC-3, researchers can examine ubiquitin-proteasome system intersections with prostate cancer progression and drug sensitivity.
This knockout cell line is suitable for applications including western blotting, RT-qPCR, cell viability, drug sensitivity, co-immunoprecipitation, and ubiquitination assays to analyze CRBN signaling and drug responses. Migration/invasion assays assess metastatic roles, and flow cytometry evaluates apoptotic or cell cycle changes. The model supports research in multiple myeloma, myelodysplastic syndromes, intellectual disability, and prostate cancer biology. For further information or technical support, please contact Ascent Research.
