The MYG1 Knockout PaTu 8988t Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the PaTu 8988t pancreatic ductal adenocarcinoma cell line, engineered to disrupt the MYG1 gene. This loss-of-function model enables investigation of MYG1-dependent mitochondrial processes and cell proliferation in a tumorigenic pancreatic epithelial context. The polyclonal format provides a diverse pool of knockout cells, reflecting a range of editing events within the target gene.
The host cell line, PaTu 8988t, is a human pancreatic ductal adenocarcinoma line originally established from a liver metastasis. It maintains key molecular characteristics of metastatic pancreatic cancer, exhibiting epithelial morphology and genetic alterations typical of pancreatic tumors. Its tumorigenic potential and retention of pancreatic epithelial identity provide a suitable cellular environment for examining the impact of MYG1 loss on mitochondrial function and cancer cell behavior.
MYG1 encodes a mitochondrial protein that participates in mitochondrial RNA metabolism and translation, modulating cellular energy homeostasis and proliferation. Mechanistically, MYG1 interacts with the HSP90 chaperone machinery and mitochondrial ribosomal subunits, and transcriptionally responds to MYC and growth factor signaling. Downstream, MYG1 influences cell cycle regulators including CDK2 and Cyclin D1, linking mitochondrial activity to cell cycle progression. Disruption of MYG1 perturbs the HSP90 chaperone cycle and impairs mitochondrial translation, leading to decreased expression of mitochondrial ribosomal proteins and altered cell cycle regulation.
In PaTu 8988t cells, MYG1 knockout disrupts mitochondrial translational fidelity and attenuates HSP90-dependent stabilization of key cell cycle drivers, reducing tumorigenic potential. This model recapitulates the dependence of pancreatic cancer cells on mitochondrial function for sustained growth and provides a system to dissect the interplay between mitochondrial metabolism and cell cycle control. The knockout population allows evaluation of MYG1 loss on proliferation, migration, and metabolic reprogramming.
This product is suitable for functional genomics and drug target validation studies, including cell proliferation assays (MTT, BrdU), migration/invasion assays, mitochondrial function analyses (Seahorse respirometry), and transcriptional profiling by RNA-seq. Protein and gene expression analyses can be performed via western blotting, immunofluorescence, RT-qPCR, and co-immunoprecipitation. These applications support investigations into pancreatic cancer biology, mitochondrial dysfunction, and MYG1 target validation. For additional details, please contact Ascent Research.
