DIS3L Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting DIS3L in the human A2780 ovarian carcinoma cell line. This loss-of-function model enables study of DIS3L, the catalytic subunit of the cytoplasmic exosome with 3′-5′ exoribonuclease activity. The polyclonal format provides a heterogeneous gene disruption pool suitable for population-level functional analyses.
The A2780 cell line is a cisplatin-sensitive human ovarian adenocarcinoma epithelial model derived from a chemotherapy-na?ve patient, widely employed to investigate oncogenic signaling and chemoresistance.
DIS3L functions as the catalytic core of the cytoplasmic exosome complex, executing 3′-5′ exoribonuclease activity essential for mRNA decay, miRNA processing, and RNA surveillance. It directly interacts with exosome subunits EXOSC2, EXOSC3, and EXOSC4, and operates alongside DIS3 and RNA helicases. CRISPR-mediated disruption eliminates exonuclease activity, impairing degradation of target mRNAs and likely causing transcriptomic dysregulation.
In A2780 ovarian cancer cells, DIS3L knockout destabilizes mRNA decay, leading to altered gene expression that may influence proliferation, apoptosis, and drug response. The inherent cisplatin sensitivity of A2780 makes this model valuable for probing whether exosome-mediated RNA metabolism contributes to chemoresistance. The interaction of DIS3L with EXOSC2, EXOSC3, and EXOSC4 further enables dissection of exosome-dependent regulatory networks in ovarian cancer.
Applications include RNA-seq to identify stabilized transcripts, RT-qPCR and mRNA stability assays for validation, and western blotting to confirm protein loss. Functional studies using cell viability, apoptosis, and drug sensitivity assays, especially with cisplatin, can elucidate roles in ovarian cancer drug resistance. This polyclonal knockout supports investigations into mRNA decay pathways, miRNA processing, and exosome biology. For further information, contact Ascent Research.
