PA-TU-8988S
Cat.No.: CSC-C0326
Species: Homo sapiens (Human)
Source: Liver Metastasis
Morphology: adherent epitheloid 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-8988S (also designated PaTu 8988s) is a well-characterized human pancreatic adenocarcinoma cell line. It was established in 1985 from a liver metastasis of a primary pancreatic adenocarcinoma in a 64-year-old female patient. The cells exhibit adherent epitheloid morphology and grow as monolayers. PA-TU-8988S harbors clinically relevant driver mutations in KRAS, SMAD4, and TP53, mirroring the genetic landscape of human pancreatic ductal adenocarcinoma.
A defining feature of PA-TU-8988S is its origin as one of two sister lines—alongside PA-TU-8988T—derived from the same metastatic lesion. While PA-TU-8988T exhibits a mesenchymal-like, spindle-shaped morphology with high ganglioside levels and low metastatic capacity, PA-TU-8988S displays an epithelial-like phenotype with preserved E-cadherin expression, cell-cell contacts, and polarity. Importantly, PA-TU-8988S is the metastatic counterpart: upon intravenous injection into nude mice, it selectively colonizes the lung, whereas PA-TU-8988T fails to metastasize. This isogenic pair provides an exceptional model for dissecting the molecular determinants of metastasis.
Chamber Gap Assay Enables Sensitive Analysis of Cancer-Induced Macrophage Migration
Pancreatic cancer ranks among the most lethal malignancies. A key contributor to its poor prognosis is the capacity of tumor cells to recruit macrophages and reprogram them into a tumor-promoting rather than tumor-eliminating phenotype. Therefore, elucidating how and why macrophages are recruited to the tumor is essential for designing new therapeutic strategies. However, widely used laboratory methods do not permit direct visualization of cell movement or accurate quantification of migration dynamics. Here, we adapted and evaluated a novel in vitro method, the Chamber Gap Assay (CGA). By culturing cancer cells and macrophages in separate but connected compartments, this system permits real-time visualization of macrophage migration toward cancer cells and the resulting morphological changes.
In the model assessing the effects of human pancreatic cancer cell lines PA-TU-8988T and PA-TU-8988S on the migration of THP-1 macrophages, we observed a time-dependent increase in THP-1 macrophage migration (Fig. 1A,B), an increased migration toward pancreatic cancer cells (Fig. 1C), and a gradual rise in the number of migrated THP-1 cells, including cells reaching migration distances beyond 500 µm (Fig. 1D).

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