The DTWD1 Knockout A2780 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal cell population derived from the A2780 human ovarian carcinoma cell line, harboring disruption of the DTWD1 gene. This polyclonal knockout pool enables loss-of-function studies of DTWD1 in a heterogeneous cell background, providing a robust tool for investigating the gene??s role in tRNA modification and cancer biology without single-cell cloning biases.
The parental A2780 cell line is an epithelial ovarian cancer model isolated from a patient with endometrioid adenocarcinoma. These cells are cisplatin-sensitive, making them suitable for examining chemosensitivity mechanisms. A2780 cells retain key ovarian cancer signaling characteristics and serve as a widely used platform for functional genomics in ovarian carcinoma research.
DTWD1 encodes a DTW domain-containing protein predicted to function as a tRNA methyltransferase in the wybutosine biosynthesis pathway. This pathway, involving enzymes such as TRMT5, TYW1, TYW2, TYW3, and TYW4, catalyzes the formation of wybutosine at position 37 of tRNA^Phe, a modification critical for maintaining ribosomal reading frame fidelity. DTWD1 is thought to contribute to a specific step in this cascade, though its precise molecular interactions and upstream regulators remain to be elucidated. Disruption of DTWD1 may impair wybutosine synthesis, resulting in hypomodified tRNA^Phe, which can promote ribosomal frameshifting and globally alter translation dynamics. Downstream consequences may include changes in the expression of proteins involved in proliferation, apoptosis, and stress responses.
In the A2780 ovarian carcinoma context, knockout of DTWD1 provides a model to dissect how tRNA modification defects influence cancer cell phenotypes. Aberrant tRNA modifications have been associated with tumorigenesis, and perturbing wybutosine biosynthesis may affect translation of specific oncogenic or tumor-suppressive mRNAs. This model can help elucidate whether translation fidelity pathways contribute to the cisplatin sensitivity of A2780 cells, as altered tRNA modifications could impact the cellular response to genotoxic stress. Thus, DTWD1 knockout in A2780 cells offers a unique entry point for studying the intersection of epitranscriptomic regulation and ovarian cancer biology.
Researchers can employ this DTWD1 polyclonal knockout model in a range of functional assays, including western blotting and RT-qPCR to confirm DTWD1 depletion, LC-MS/MS-based analysis of tRNA modifications, cell proliferation and apoptosis assays, and cisplatin sensitivity profiling. Polysome profiling can evaluate global translation effects, while migration and invasion assays allow assessment of metastatic potential. This product is also suitable for drug sensitivity panels and functional genomics screens targeting the tRNA modification machinery. For further details or custom inquiries, please contact Ascent Research.
