The DRAM2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous knockout cell population generated from the A2780 human ovarian carcinoma line via CRISPR/Cas9-mediated disruption of the DRAM2 gene. This polyclonal pool provides a robust loss-of-function model capturing a spectrum of mutations, avoiding clonal selection biases and enabling rigorous investigation of DRAM2-dependent autophagy and apoptosis pathways.
The A2780 cell line is an epithelial ovarian carcinoma model established from an untreated patient. It represents an ovarian surface epithelial-derived tumor with well-characterized oncogenic properties and is widely employed for studying tumor suppressor mechanisms, chemotherapy responses, and signaling networks relevant to ovarian cancer.
DRAM2 encodes a lysosomal protein transcriptionally activated by TP53 in response to DNA damage or retinoic acid. It promotes macroautophagy and apoptosis through direct interactions with LC3, LAMP1, and the autophagic adapter p62/SQSTM1. DRAM2 facilitates lysosomal membrane permeabilization and caspase activation, and its activity intersects with mTOR signaling and the pro-apoptotic factor BAX, linking p53-regulated pathways to cell death execution.
In the A2780 background, DRAM2 knockout enables dissection of its roles in autophagy-mediated survival and apoptotic signaling. The polyclonal nature mirrors tumor heterogeneity, facilitating studies on cisplatin sensitivity and autophagy pathway dependencies. This model supports evaluation of DRAM2 as a tumor suppressor and identification of synthetic lethal interactions with autophagy components such as ATG5.
These polyclonal knockout cells are suitable for western blotting of DRAM2 and autophagy markers, RT-qPCR, LC3 puncta formation assays, Annexin V apoptosis assays, MTT viability tests, colony formation assays, and cisplatin sensitivity profiling. Applications include functional genomics screens, autophagy-targeted drug discovery, and retinoic acid signaling studies. For more information, contact Ascent Research.
