This product provides a polyclonal population of MES-OV ovarian clear cell carcinoma cells with CRISPR/Cas9-mediated disruption of DUSP23. The polyclonal knockout pool offers a heterogeneous loss-of-function model for studying this atypical dual-specificity phosphatase in a tumorigenic epithelial background, suitable for experiments where population-level effects are informative.
The parental MES-OV cell line is derived from human ovarian clear cell carcinoma, a distinct histological subtype of epithelial ovarian cancer. These tumorigenic epithelial cells endogenously express MAP kinase signaling components and respond to mitogenic and stress cues, offering a relevant model for studying ovarian cancer biology and the role of DUSP23 in this context.
DUSP23 is an atypical dual-specificity phosphatase that dephosphorylates MAP kinases (ERK1/2, JNK, p38) by targeting conserved threonine and tyrosine residues, thereby attenuating kinase activity. Upstream signals such as growth factors, cellular stress, reactive oxygen species, and EGFR ligands trigger its regulatory function. Downstream, DUSP23-mediated dephosphorylation reduces activation of transcription factors (c-Jun, c-Fos, ATF2) and alters expression of cycle regulators cyclin D1 and p21. The phosphatase interacts with MAP kinases, scaffold proteins, and 14-3-3 proteins, integrating into RAS-RAF-MEK-ERK, JNK, and p38 cascades to modulate proliferation and stress responses.
In ovarian clear cell carcinoma, dysregulated MAPK signaling drives uncontrolled growth. DUSP23 knockout in MES-OV cells allows investigation of how loss of this phosphatase shifts kinase activity balance. Without DUSP23, phosphorylation of ERK1/2, JNK, and p38 is expected to become elevated upon stimulation, leading to altered transcriptional programs and phenotypes. This model is instrumental for dissecting compensatory mechanisms and MAPK pathway dependencies in ovarian cancer cell proliferation and survival.
Applications include western blotting for phospho-ERK/JNK/p38 to assess MAPK activity, RT-qPCR and immunofluorescence for DUSP23 expression, and functional assays like proliferation, colony formation, and wound healing. Flow cytometry and co-immunoprecipitation can further characterize cell cycle changes and protein interactions. This polyclonal knockout model also suits functional genomics screens for synthetic lethal interactions. For additional product information, please contact Ascent Research.
