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YAPC
Cat.No.: CSC-C0430
Species: Human
Source: pancreas carcinoma
Morphology: cobblestone-like 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
The YAPC cell line was developed in 1993 by the National Center for Global Health and Medicine, Japan from the ascites of a 43-year-old male patient with untreated advanced pancreatic cancer. YAPC cells are adherent and autocrine IL-1α-dependent for proliferation. Immunophenotypically, YAPC is positive for several adhesion molecules including cytokeratin, EpCAM, and vimentin and exhibits typical epithelial morphology. Genotypically, YAPC is near-triploid (8% polyploid) and has several chromosomal deletions and translocations associated with pancreatic cancer. Because of its natural resistance to cisplatin (24 h IC50 > 100 µM), YAPC is commonly used in drug development and research as an in vitro model for drug resistance, drug screening and drug combination research. YAPC has been used to screen novel platinum/organometallic compounds, 3D tumor spheroid invasion, KRAS-targeted therapy, Wnt/β-catenin signaling and the mitochondrial apoptosis pathway, among many others.
Cytotoxicity of Cisplatin in Pancreatic Tumor Lines
Pancreatic ductal adenocarcinoma (PDAC) is highly lethal and chemoresistant; gemcitabine frequently fails and cisplatin shows variable efficacy. Muscella et al. aimed to clarify why four genotypically distinct PDAC (BxPC-3, Mia-Paca-2, PANC-1, and YAPC) lines respond differently to cisplatin, with the goal of identifying molecular determinants of resistance. They treated the four lines with 0.1–200 µM cisplatin and measured viability by SRB (validated by cell counts). Figure 1 and Supplementary Table S1 show a dose- and time-dependent drop in survival: BxPC-3 and MIA PaCa-2 were most sensitive (IC50 = 5.96 ± 2.32 µM and 7.36 ± 3.11 µM at 48 h), whereas YAPC and PANC-1 were resistant (IC50 = 56.7 ± 9.52 µM and 100 ± 7.68 µM). Subsequent work focused on the contrasting pair BxPC-3 and YAPC.
Fig. 1. Cytotoxic effects of cisplatin on pancreatic tumor lines. BxPC-3 (A), Mia Paca-2 (B), PANC-1 (C) and YAPC (D) cells were treated with different concentration of cisplatin (Muscella A, Cossa LG, et al., 2024).
[Pt(η1-C2H4-OMe)(DMSO)(phen)]+ (1) and [Pt(η1-C2H4-OEt)(DMSO)(phen)]+ (2) Inhibition of PDAC Cell Growth
PDAC chemoresistance limits cisplatin efficacy. Three human PDAC lines (Mia PaCa-2, PANC-1, YAPC) were exposed to complexes 1 and 2 or cisplatin; SRB, apoptosis, cell-cycle, mitochondrial membrane potential, and 3D-spheroid migration assays were employed. The goal was to determine if 1 and 2 display superior antiproliferative and antimetastatic effects versus cisplatin. SRB assay on Mia PaCa-2, PANC-1 and YAPC showed both [Pt(η1-C2H4-OR)(DMSO)(phen)]+ complexes (R = Me, 1; Et, 2) killed cells in a concentration-dependent manner (0–100 µM, Fig. 2). After 24 h, 1 and 2 were markedly more potent than cisplatin (IC50 9.15–31.6 µM vs >100 µM for PANC-1; Fig. 3). Only Mia PaCa-2 displayed lower IC50 for cisplatin (3.76 ± 1.11 µM) at 48 h (Fig. 2b, Fig. 3). Chain length (Me vs Et) had minimal impact.
Fig. 2. Cytotoxic efects of cisplatin, [Pt(η1-C2H4-OMe)(DMSO)(phen)]+(1), [Pt(η1-C2H4-OEt)(DMSO)(phen)]+ (2) (Stefàno E, Cossa L G, et al., 2023).
Fig. 3. IC50 values were calculated and presented as means ± standard deviation. Letters indicate IC50 values that are significantly lower (p < 0.05) than those of cisplatin (c), 1 (m), and 2 (e) at the same time point (Stefàno E, Cossa L G, et al., 2023).
To detach adherent cells from the culture surface, various methods can be used. These include enzymatic methods using enzymes like trypsin or collagenase, physical methods like scraping or shaking or using commercially available cell dissociation reagents.
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