The CCNY Knockout A2780 Polyclonal Cells represent a heterogeneous population of human ovarian carcinoma A2780 cells in which the CCNY gene has been disrupted via CRISPR/Cas9-mediated genome editing. This polyclonal knockout pool provides a loss-of-function model for studying cyclin Y-dependent processes without the selective pressure of clonal isolation, preserving natural genetic diversity. The product is supplied as a ready-to-use cell population suitable for a wide range of functional assays in cancer biology and signal transduction research.
The A2780 cell line is derived from an ovarian endometrioid adenocarcinoma of an untreated patient and is characterized by its epithelial morphology and sensitivity to cisplatin. As an established model of epithelial ovarian carcinoma, A2780 cells retain key features of high-grade serous ovarian cancer, including functional p53 and BRCA1/2 status. Their cisplatin-sensitive nature makes them particularly valuable for investigating mechanisms of chemoresistance and for screening therapeutic strategies aimed at restoring drug sensitivity.
At the molecular level, CCNY encodes cyclin Y, a regulatory subunit that assembles with the cyclin-dependent kinase CDK14 to form an active kinase complex. In response to upstream cues including Wnt3a and the transcription factor E2F1, the cyclin Y?CCDK14 complex directly phosphorylates the Wnt co-receptor LRP6 on its intracellular domain. This phosphorylation event triggers the recruitment of Axin and disassembly of the ??-catenin destruction complex, leading to ??-catenin stabilization and nuclear translocation. Nuclear ??-catenin interacts with TCF/LEF transcription factors to promote the expression of Wnt target genes such as MYC and CCND1, which drive G1/S cell cycle progression and cellular proliferation.
In the context of ovarian carcinoma, deregulated Wnt/??-catenin signaling is frequently implicated in tumor initiation, maintenance, and chemoresistance. The A2780 cell line, with its well-defined cisplatin sensitivity, provides a relevant background for dissecting the contributions of cyclin Y to ovarian cancer biology. Loss of CCNY in these cells is expected to attenuate LRP6 phosphorylation and ??-catenin-driven transcriptional programs, thereby allowing researchers to explore how this axis influences cell cycle progression, proliferation, and response to platinum-based chemotherapy. This knockout model is thus a valuable tool for interrogating Wnt-dependent mechanisms of drug resistance and identifying downstream effectors that could serve as therapeutic vulnerabilities.
Typical experimental applications include monitoring changes in ??-catenin levels and subcellular localization by immunofluorescence and western blotting following Wnt3a stimulation, as well as evaluating transcriptional responses of MYC and CCND1 via RT-qPCR. The polyclonal knockout population is well suited for cell proliferation assays and cisplatin sensitivity testing, enabling dose?Cresponse studies under Wnt-modulating conditions. By providing a loss-of-function system for cyclin Y in a clinically relevant ovarian cancer cell line, this product supports mechanistic studies of the Wnt/??-catenin pathway in cell cycle control and drug resistance. For additional information, please contact Ascent Research.
