The ATAD3A Knockout A2780 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ATAD3A gene in the human A2780 ovarian carcinoma cell line. This loss-of-function model is generated using CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous population of cells with targeted disruption of ATAD3A. The polyclonal format preserves population-level genetic diversity while enabling robust functional studies of ATAD3A-dependent processes. This product is suitable for researchers investigating mitochondrial biology, ovarian cancer pathology, and drug resistance mechanisms.
The host cell line A2780 is an epithelial ovarian cancer cell line originally established from an untreated patient with ovarian endometrioid adenocarcinoma. A2780 cells are widely used as a model system for ovarian cancer research, particularly for studying chemosensitivity and resistance, as they retain key features of the original tumor microenvironment. Their epithelial origin makes them relevant for investigations into mitochondrial function in ovarian carcinoma progression and therapy response.
ATAD3A encodes a mitochondrial inner membrane protein that plays a critical role in mitochondrial dynamics, cholesterol transport, and mitochondrial DNA (mtDNA) maintenance. ATAD3A interacts with key mitochondrial fusion proteins MFN2 and OPA1, and components of the MICOS complex, linking mitochondrial architecture to cristae organization. The protein is regulated upstream by transcription factor MYC and by cellular stress signals such as oxidative stress and cholesterol depletion. Downstream, ATAD3A influences mitochondrial membrane potential, reactive oxygen species (ROS) production, ATP synthesis, and the balance of pro- and anti-apoptotic Bcl-2 family members. This network positions ATAD3A as a central node in mitochondrial homeostasis and apoptosis signaling.
In the A2780 ovarian cancer context, ATAD3A knockout disrupts mitochondrial cholesterol trafficking and mtDNA homeostasis, leading to impaired mitochondrial function and increased susceptibility to apoptosis. Given that ATAD3A overexpression has been associated with chemoresistance in ovarian cancer, this knockout model may exhibit reduced tumor cell viability and enhanced sensitivity to chemotherapeutic agents. The dysregulation of mitochondrial dynamics and activation of the mitochondrial unfolded protein response further underscore the utility of this model for mechanistic studies of mitochondrial stress pathways in cancer cells.
This polyclonal knockout cell population is a valuable tool for a variety of research applications, including the study of ovarian cancer drug resistance, mitochondrial dysfunction in cancer, cholesterol metabolism in tumor cells, mtDNA instability, and apoptosis signaling. Researchers can employ representative assays such as western blotting, RT-qPCR, immunofluorescence, flow cytometry, apoptosis assays, drug sensitivity assays, mitochondrial membrane potential measurements, and ATP assays to characterize the functional consequences of ATAD3A loss. For further information or to discuss custom applications, please contact Ascent Research.
