The ATAD3A Knockout KYSE-150 Polyclonal Cells product offers a polyclonal pool of KYSE-150 esophageal squamous carcinoma cells with CRISPR/Cas9-mediated disruption of the ATAD3A gene. This heterogeneous knockout population provides a loss-of-function model while avoiding the clonal bias of single-cell-derived lines, allowing studies in a genetically diverse context representative of tumor heterogeneity.
KYSE-150 is a poorly differentiated esophageal squamous cell carcinoma cell line isolated from a Japanese patient. As a malignant epithelial model, it recapitulates aggressive cancer features, including aberrant proliferation and migration, and serves as a standard in vitro system for esophageal cancer research and therapeutic testing.
ATAD3A is a mitochondrial inner membrane AAA+ ATPase that acts as a tethering factor at ER?Cmitochondria contact sites, regulating cholesterol trafficking and mitochondrial fission. It is transcriptionally induced by MYC and integrated into p53 and Wnt/??-catenin signaling networks. ATAD3A directly binds DRP1, MFN2, and HSP60 to control mitochondrial dynamics, and it interacts with VDAC and BAX to modulate apoptosis. Moreover, ATAD3A promotes SREBP-dependent cholesterol gene expression. Consequently, its disruption impairs mitochondrial morphology, alters ER?Cmitochondrial communication, and sensitizes cells to intrinsic apoptosis.
In KYSE-150 cells, ATAD3A is typically overexpressed and supports tumorigenic processes. Its knockout disrupts mitochondrial fission/fusion equilibrium, likely causing mitochondrial fragmentation and metabolic stress. Loss of ER?Cmitochondrial contacts and cholesterol handling further compromises survival signaling, attenuating proliferation and enhancing apoptotic susceptibility. This model thus enables dissection of ATAD3A-driven oncogenic mechanisms, including mitochondrial adaptations that sustain esophageal cancer cell viability and treatment resistance.
This polyclonal knockout model is suitable for diverse assays: Western blotting of ATAD3A and its partners (DRP1, MFN2, VDAC); immunofluorescence with MitoTracker or TOM20 to assess mitochondrial morphology; RT-qPCR of SREBP targets and mitochondrial genes; apoptosis assays (Annexin V/PI); cholesterol quantification; co-immunoprecipitation of ATAD3A?CDRP1 interactions; and functional studies including MTT proliferation, scratch wound healing, and Transwell invasion. For inquiries, please contact Ascent Research.
