Genome-edited Cells
Breast (mammary gland)
The CT83 Knockout MDA-MB-231 Cell Line is a CRISPR/Cas9-edited knockout human triple-negative breast cancer (TNBC) cell line targeting CT83 (cancer/testis antigen 83). MDA-MB-231 is a highly invasive, mesenchymal-like epithelial line lacking ER, PR, and HER2, and harboring mutant p53 and KRAS G13D, making it an ideal model for metastatic TNBC research. CT83 activates PI3K/AKT and MAPK/ERK signaling, upregulating Cyclin D1, Bcl-2, and MMP2/MMP9 to drive proliferation and invasion. This knockout model supports applications in cancer immunotherapy, target validation, and functional studies of CT83-dependent pathways using assays such as western blot, proliferation, migration, and xenograft models.
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The CT83 Knockout MDA-MB-231 Cell Line is a CRISPR/Cas9-edited human cell line designed for constitutive disruption of the CT83 gene in the MDA-MB-231 triple-negative breast cancer background. This loss-of-function model enables precise investigation of CT83’s roles in tumorigenesis and metastasis without wild-type gene interference, providing a reliable tool for functional genomics and drug target studies. Supplied as a stable knockout cell line, it is suitable for a broad range of in vitro and in vivo experimental systems.
MDA-MB-231 is a highly invasive, mesenchymal-like epithelial breast adenocarcinoma cell line derived from a metastatic pleural effusion. It lacks estrogen receptor, progesterone receptor, and HER2 amplification, and harbors mutant p53 and KRAS G13D. These features render it a classical in vitro and in vivo model for metastatic triple-negative breast cancer, particularly suited for studying the molecular drivers of invasion and dissemination.
CT83 (KK-LC-1) is a cancer/testis antigen normally restricted to testis but aberrantly expressed in multiple cancers. It promotes cell proliferation, migration, and invasion by activating both the PI3K/AKT and MAPK/ERK pathways. CT83 expression is upregulated by SOX2 and ETS transcription factors, often via DNA hypomethylation. Downstream, it transcriptionally induces Cyclin D1 (CCND1) to drive cell cycle progression, BCL2 to enhance survival, and MMP2/MMP9 to degrade the extracellular matrix, all mediated through key kinases including PIK3CA, AKT1, mTOR, RAF1, MEK, and ERK. CT83 may also influence cytoskeletal organization, further potentiating cell motility. Ectopic expression of CT83 has been documented in triple-negative breast cancer, non-small cell lung cancer, gastric adenocarcinoma, ovarian cancer, and melanoma, underscoring its relevance across multiple tumor types.
In MDA-MB-231 cells, CT83 knockout is anticipated to impair the aggressive phenotype, as the gene’s signaling outputs converge on critical nodes of proliferation and invasion. This model allows researchers to dissect CT83-dependent contributions to TNBC metastasis and evaluate its potential as an immunotherapeutic target, given its restricted expression profile and immunogenicity. Pairing knockout and parental lines facilitates high-resolution comparative analyses of signaling networks, epigenetic regulation, and immune recognition.
Applications include target validation, cancer-testis antigen biology, and biomarker development. Typical assays with this cell line encompass Western blotting for CT83, phosphorylated AKT and ERK, and Cyclin D1; RT-qPCR for transcript quantification; MTT or CCK-8 proliferation assays; Transwell migration/invasion tests; apoptosis measurements via flow cytometry; RNA-seq for global expression profiling; and xenograft tumor growth studies. Together, these enable comprehensive functional and translational research. For further information, please contact Ascent Research.
