In Stock Cell Lines
Mus musculus (Mouse)
Large intestine (colon)
Adherent
The Kdm3a Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited murine colorectal carcinoma cell line with targeted disruption of the Kdm3a gene. KDM3A is a histone H3K9me1/2 demethylase and transcriptional coactivator that regulates Wnt/??-catenin and hypoxia-responsive gene expression by interacting with ??-catenin and promoting transcription of downstream targets like CCND1 and MYC. This loss-of-function model is valuable for studying epigenetic regulation of colorectal cancer growth, metastasis, metabolic reprogramming, and drug target validation. Assays such as ChIP-qPCR, RT-qPCR, RNA-seq, and cell proliferation, migration, and metabolic analyses can be performed. Please contact Ascent Research for further details.
CISD1 Knockout Hela Polyclonal Cells
Cat. No. ARG8781
ITGAE Knockout Raji Polyclonal Cells
Cat. No. ARG23841
ARID4B Knockout A2780 Polyclonal Cells
Cat. No. ARG28770
NIPSNAP1 Knockout MES-OV Polyclonal Cells
Cat. No. ARG5890
MAPK3 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4313
DDX60L Knockout AGS Polyclonal Cells
Cat. No. ARG2204
The Kdm3a Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited knockout cell line engineered to disrupt the Kdm3a gene in the murine CT26.WT colorectal carcinoma background. This loss-of-function model enables investigation of KDM3A-dependent epigenetic regulation and its role in tumor cell biology. By abolishing KDM3A expression, researchers can directly examine the consequences of impaired histone H3K9me1/2 demethylation in a genetically defined cancer cell context.
The CT26.WT cell line is a well-characterized murine colon carcinoma model derived from BALB/c mice following chemical induction with N-nitroso-N-methylurethane. It is widely utilized in colorectal cancer and immunotherapy research due to its syngeneic compatibility and reproducible tumor growth. The parental CT26.WT line retains key signaling pathway activities relevant to human colorectal cancer, making it a suitable host for targeted gene disruption studies.
KDM3A (lysine demethylase 3A) functions as a histone H3K9me1/2 demethylase and transcriptional coactivator, regulating chromatin accessibility and gene expression programs. It is activated by upstream signals including androgen receptor, HIF1A, TGF-??, and Wnt/??-catenin, and interacts with ??-catenin, CREB-binding protein (CBP), and Sp1 to drive transcription of downstream targets such as CCND1, MYC, SREBF1, GLUT1, and VEGF. KDM3A-mediated H3K9me1/2 demethylation relieves repressive chromatin marks, thereby facilitating activation of genes involved in cell proliferation, metabolism, and hypoxia response.
In CT26.WT colorectal carcinoma cells, KDM3A knockout eliminates its demethylase activity, leading to increased repressive H3K9me1/2 methylation at promoters of Wnt/??-catenin and hypoxia-responsive genes. This epigenetic silencing results in downregulation of critical oncogenic effectors including CCND1 and MYC, suppressing cell cycle progression and metabolic reprogramming. Consequently, KDM3A-deficient CT26.WT cells exhibit reduced proliferation, colony formation, migration, and tumorigenic potential, highlighting KDM3A as a key mediator of colorectal cancer aggressiveness.
This knockout cell line is suitable for a wide range of research applications, including dissecting epigenetic regulation of colorectal tumor growth and metastasis, functional analysis of histone demethylases, Wnt/??-catenin pathway interrogation, drug target validation, and study of metabolic reprogramming in cancer. Researchers can employ assays such as ChIP-qPCR for H3K9me2 enrichment at target gene promoters, RT-qPCR for transcript quantification (Ccnd1, Myc, Glut1), RNA-seq for whole-transcriptome profiling, cell proliferation and colony formation assays, Transwell migration/invasion assays, and metabolic flux analyses (glucose uptake, lactate production). For additional information or technical support, please contact Ascent Research.
