The ATAD3A Knockout PaTu 8988t Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt ATAD3A gene expression in the human pancreatic ductal adenocarcinoma cell line PaTu 8988t. This loss-of-function model is generated using CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous pool of cells with targeted inactivation of ATAD3A. The polyclonal format provides a robust and physiologically relevant population for studying mitochondrial biology and cancer-related processes without the clonal bias inherent in single-cell-derived lines.
The host cell line PaTu 8988t is an established epithelial cell line derived from a liver metastasis of a pancreatic ductal adenocarcinoma. It retains key characteristics of the original tumor, including adherent growth, tumorigenic properties, and metastatic potential. These cells serve as a valuable model system for dissecting the molecular mechanisms underlying pancreatic cancer progression, metastasis, and drug resistance, particularly within the context of mitochondrial function and stress responses.
ATAD3A encodes a mitochondrial inner membrane ATPase that acts as a critical regulator of mitochondrial dynamics and cholesterol homeostasis. Mechanistically, ATAD3A inhibits DRP1-mediated mitochondrial fission and modulates intrinsic apoptosis signaling. Its activity is governed by upstream regulators such as HSF1, MYC, and mitochondrial stress signals, and it functions downstream to control cytochrome c release, mitochondrial DNA replication, and oxidative phosphorylation complex assembly. ATAD3A interacts directly with key mitochondrial proteins including DRP1, mitofilin (IMMT), prohibitins, and components of the MICOS complex, as well as the calcium-binding protein S100B. Within mitochondrial dynamics pathways, it operates alongside DRP1, MFN1, MFN2, OPA1, BAX, cytochrome c, and the cholesterol transporter StAR.
In PaTu 8988t cells, ATAD3A contributes to mitochondrial stability and chemoresistance, characteristics that are particularly relevant to pancreatic cancer biology. Disruption of ATAD3A in this metastatic cell background provides a powerful tool to investigate how mitochondrial architecture and cholesterol trafficking influence tumor cell survival, apoptotic threshold, and response to chemotherapeutic agents such as gemcitabine. The knockout model thus enables dissection of the molecular interplay between mitochondrial quality control and pancreatic cancer aggressiveness.
This product supports a wide range of research applications, including the investigation of mitochondrial dynamics, chemoresistance mechanisms, and mitochondrial stress responses in pancreatic cancer. Researchers can employ these cells in immunofluorescence-based mitochondrial morphology assays, JC-1 mitochondrial membrane potential measurements, ATP production analyses, and cytochrome c release assays. Additionally, they are suitable for co-immunoprecipitation studies of ATAD3A-DRP1 interactions, Seahorse metabolic flux analysis, and gemcitabine sensitivity testing, facilitating drug screening and functional genomics studies. For further information or to discuss custom applications, please contact Ascent Research.
