The DUS3L Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, designed to disrupt the DUS3L gene locus. This product provides a heterogeneous pool of cells with targeted disruption of DUS3L, enabling loss-of-function studies in a polyclonal background. The knockout population is generated using CRISPR/Cas9-mediated gene disruption, resulting in a mixed population of edited alleles that collectively represent functional DUS3L ablation.
A2780 is a well-characterized human epithelial ovarian carcinoma cell line isolated from an untreated patient, widely utilized in cancer biology and pharmacology for its inherent sensitivity to cisplatin. This cell line serves as a robust model for studying mechanisms of chemosensitivity and resistance, as well as ovarian carcinoma progression and metastasis. The epithelial origin and reliable growth characteristics of A2780 make it an ideal host for genetic manipulation to interrogate gene function in ovarian cancer.
DUS3L encodes a putative dual-specificity phosphatase (DUSP) capable of dephosphorylating phosphotyrosine and phosphoserine/threonine residues, placing it among regulators of MAP kinase signaling. Mechanistically, DUS3L is proposed to dephosphorylate and inactivate key MAP kinases including ERK1/2 and JNK, thereby attenuating signal transduction through the RAS-RAF-MEK-ERK cascade and JNK-mediated pathways. This negative feedback regulation may be triggered by MAPK pathway activation and oxidative stress, positioning DUS3L as a critical modulator of cellular responses to mitogenic and stress signals. Predicted by homology, DUS3L interacts directly with ERK1/2 and JNK, fine-tuning their activity to control cell proliferation, survival, and apoptosis.
Given the central role of MAPK signaling in ovarian cancer cell fate and drug response, the DUS3L knockout in A2780 cells offers a valuable system to dissect the phosphatase??s contribution to cisplatin sensitivity. Dysregulation of ERK and JNK activity is frequently associated with chemoresistance, and DUS3L may serve as a negative regulator whose loss promotes sustained MAPK activation, altering apoptotic thresholds and cell survival. This knockout model enables precise assessment of how DUS3L disruption impacts basal and cisplatin-induced signaling dynamics, proliferation, and apoptosis in an epithelial ovarian cancer background.
Researchers can employ this polyclonal knockout population to investigate DUS3L function in MAPK regulation via phospho-ERK and phospho-JNK western blot analysis, assess cell viability and apoptosis using MTT and Annexin V assays, and determine cisplatin IC50 shifts upon DUS3L ablation. Functional studies may also include migration and invasion transwell assays to evaluate metastatic potential. These applications support target validation, drug discovery, and mechanistic studies of ovarian cancer chemoresistance. For further information or to request this model, please contact Ascent Research.
