PA-TU-8902
Cat.No.: CSC-C0312
Species: Homo sapiens (Human)
Source: Pancreas
Morphology: epithelial adherent cells growing in monolayers
Culture Properties: monolayer
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Immunology: cytokeratin +, cytokeratin-7 +, cytokeratin-8 +, cytokeratin-17 -, cytokeratin-18 +, cytokeratin-19 +, desmin -, endothel -, EpCAM +, GFAP -, neurofilament -,
PA-TU-8902 is a human pancreatic ductal adenocarcinoma (PDAC) cell line, established in 1985 from a primary grade II tumor of a 44-year-old female. Its paramount scientific advantage lies in its genuinely metastatic phenotype: unlike most PDAC lines that fail to colonize distant organs in vivo, PA-TU-8902 consistently forms lung, esophageal, and pleural metastases upon intravenous injection in nude mice, faithfully recapitulating late-stage human disease.
Genetically, the line harbors endogenous KRAS and TP53 mutations-the two cardinal drivers of human PDAC-while remaining negative for EBV, HBV, HCV, HIV, and HTLV, ensuring biosafety for in vivo experimentation. Its well-characterized pseudotetraploid karyotype, authenticated STR profile, and documented secretion of urokinase, cathepsins B/D, and cytokines (e.g., EpCAM+) position it as a mechanistically tractable platform for studying protease-driven invasion, cancer cachexia, and tumor-stroma crosstalk.
Furthermore, PA-TU-8902 exhibits exceptional amenability to genetic engineering. It has been successfully deployed for CRISPR/Cas9-mediated SMAD4 knockout to dissect TGF-β signaling and mitophagy-driven chemoresistance, and engineered to stably co-express GFP, luciferase, and chicken ovalbumin (OVAL) for in vivo imaging and immunotherapy modeling. With a manageable doubling time (25-40 h) and negative mycoplasma status, PA-TU-8902 remains a reference standard for translational PDAC research spanning metastasis biology, drug resistance, and preclinical therapeutic screening.
Decitabine-Olaparib Synergistically Targets dKRAS-PDAC
Pancreatic ductal adenocarcinoma (PDAC) shows limited response to chemotherapy, partly due to the absence of effective biomarkers for personalized treatment. Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are found in 90% of PDAC cases, and tumors dependent on KRAS (dKRAS) can be identified using gene expression signature scores. Previous research indicates that dKRAS-PDAC cells are sensitive to decitabine (DEC), an FDA-approved drug for hematological cancers, though its use in solid tumors is limited by side effects.
We discovered that low-dose DEC combined with the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib (OLA) enhances antitumor activity in dKRAS-PDAC. The combination was especially effective in dKRAS-PDAC with a BRCA2 mutation, preventing metastasis growth.

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