BTK Knockout A2780 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the gene encoding the Bruton??s tyrosine kinase (BTK) has been disrupted within the human ovarian carcinoma A2780 cell line. This product provides a heterogeneous pool of cells harboring CRISPR/Cas9-mediated gene disruption at the population level, enabling loss-of-function studies free from clonal selection artifacts. The polyclonal format is especially useful for robust, biologically averaged assessments of BTK-dependent phenotypes, ensuring that observed cellular responses reflect the entire gene-edited pool rather than a single clone. Researchers employing this model benefit from a versatile platform to interrogate BTK signaling outside conventional B-cell lineages, directly in an epithelial ovarian cancer context.
A2780 is a well-characterized human epithelial cell line derived from an untreated patient with endometrioid adenocarcinoma of the ovary. Widely adopted as a model for ovarian cancer research, A2780 cells retain hallmark features of ovarian carcinoma, including intact signaling cascades and proliferative capacity. The cell line??s origin from an untreated tumor provides a valuable baseline for investigating intrinsic molecular vulnerabilities and responses to targeted therapies. In the context of BTK knockout, the A2780 background allows exploration of non-hematopoietic functions of BTK, whose aberrant expression has been detected in solid tumors, potentially contributing to oncogenic signaling networks beyond its canonical role in B-cell malignancies.
BTK is a non-receptor tyrosine kinase critically positioned downstream of the B-cell receptor (BCR) and upstream of key survival and proliferative pathways. Upon BCR engagement, SRC family kinases such as LYN and SYK phosphorylate and activate BTK, which in turn phosphorylates phospholipase C gamma 2 (PLCG2), triggering calcium mobilization and downstream activation of NF-??B and MAPK cascades (ERK, JNK, p38). BTK also integrates signals from chemokine receptors (e.g., CXCR4) and Toll-like receptors, and forms complexes with adaptor proteins including BLNK (SLP-65) and GAB1. These interactions culminate in the regulation of transcriptional targets such as MYC and the anti-apoptotic factor BCL-XL, positioning BTK as a central node in B-cell development, proliferation, and survival. Although primarily associated with hematopoietic signaling, these mechanistic connections provide a framework for examining BTK in non-hematological contexts when ectopically expressed.
In the A2780 ovarian carcinoma background, BTK knockout offers a unique opportunity to dissect the kinase??s potential contributions to solid tumor biology. While BTK is best known for its role in B-cell malignancies like chronic lymphocytic leukemia and mantle cell lymphoma, emerging evidence suggests that its aberrant expression in epithelial cancers may influence tumor cell proliferation, migration, and drug resistance. This polyclonal knockout model enables unbiased interrogation of such functions, allowing researchers to assess how loss of BTK alters ovarian cancer cell behavior in vitro. The model is particularly valuable for evaluating the efficacy and mechanism of action of BTK inhibitors, including ibrutinib and acalabrutinib, in a solid tumor context where these drugs are being investigated for repurposing.
Typical research applications for these BTK knockout A2780 polyclonal cells include functional characterization of BTK in ovarian cancer, drug sensitivity profiling, and mechanistic studies of signal transduction. Researchers may employ Western blotting to confirm BTK depletion and reduced phosphorylation of downstream targets such as PLCG2. Cell viability (MTT, CellTiter-Glo) and apoptosis (Annexin V/7-AAD) assays can quantify growth and survival effects, while Transwell assays enable assessment of migratory and invasive properties. RNA sequencing offers transcriptome-wide insights into BTK-dependent gene expression programs. These cells also serve as an excellent control for drug screens and for studying resistance mechanisms to BTK inhibitors. For further information, please contact Ascent Research.
