The DNMT3A Knockout SK-OV-3 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout population for studying DNA methyltransferase 3 alpha (DNMT3A) in ovarian cancer. This loss-of-function model was generated by CRISPR/Cas9-mediated disruption of DNMT3A in SK-OV-3 cells, yielding a heterogeneous pool with targeted gene ablation. The polyclonal format enables study of DNMT3A-dependent epigenetic regulation without clonal selection artifacts.
SK-OV-3 is an epithelial-like human ovarian cancer cell line derived from the ascites of a female patient with metastatic serous cystadenocarcinoma. The cells carry a mutant p53 gene and are widely used as a model for high-grade serous ovarian carcinoma. Their tumorigenic properties and characterized signaling networks provide a relevant background for gene function studies.
DNMT3A is a de novo DNA methyltransferase that establishes methylation patterns by catalyzing CpG methylation using S-adenosyl methionine (SAM). Its activity is governed by upstream signals including IL-6/STAT3, PI3K/AKT, and RAS/MAPK pathways, and transcription factors SP1 and AP-1. DNMT3A forms complexes with DNMT3L, UHRF1, DNMT1, HDAC1/2, and EZH2 to mediate gene silencing. Key downstream targets include tumor suppressors CDKN2A, MLH1, and BRCA1, and developmental HOX gene clusters.
Disruption of DNMT3A in SK-OV-3 eliminates de novo methyltransferase activity, causing global hypomethylation and reactivation of silenced tumor suppressors. This epigenetic shift can reverse malignant phenotypes such as proliferation, migration, and invasion, and may resensitize cells to chemotherapy. The knockout model thus permits dissection of DNMT3A??s role in maintaining oncogenic DNA methylation and assessing the functional impact of demethylation in ovarian cancer.
This polyclonal DNMT3A knockout cell pool is suitable for diverse applications including bisulfite sequencing, global methylation ELISA, RT-qPCR, ChIP-qPCR, and phenotypic assays for proliferation, apoptosis, and migration/invasion. It can be used in drug screens with demethylating agents like 5-aza-2??-deoxycytidine and in functional genomics to map DNMT3A-dependent networks. For more information, contact Ascent Research.
