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Table 2 Principal data regarding the role of PCSCs in the induction of treatment resistance

From: The epithelial to mesenchymal transition (EMT) and cancer stem cells: implication for treatment resistance in pancreatic cancer

Experimental approach Molecular characteristics of PCSCs References
Isolated SP(side population) cell fractions in L3.6pl cell‚ gemcitabine- and 5-FU-resistant L3.6pl cells were established Induce faster and more aggressive orthotopic tumor growth with higher rates of metastases‚ gemcitabine resulted in an increase of CD24 positive cells and the percentage of SP cells [117]
Incubated in the presence of 5- fluorouracil (5-FU) for 24 h, and further incubated without 5-FU for 28 days to eliminate 5-FU-sensitive cells. Certain stemness-genes such as OCT4 and NANOG were enhanced and spheres arose [118]
Treat Capan-1 and Panc-1 cells with serial concentrations of gemcitabine and counting surviving cells after 6 days, Stem markers CD44,CD24,CD133,EpCAM,Oct4 and PDX1 increased [119]
Xenograft tumours were dissociated into single cells and identified SP cells using FACS analysis SP displayed higher sphere-forming capacity, epithelial-mesenchymal transition and gemcitabine reisistant [120]
Konckdown of ALDH1 in MIA PaCa-2 cell The IC50 of gemcitabine decreased, induction of apoptosis and S-phase arrest by gemcitabine. [121]
Enriched pancreatic cancer stem CD44+/CD24+ cells in PANC-1 cells under sphere forming conditions Increased resistance to gemcitabine, migration ability, exhibit Epithelial to Mesenchymal Transition (EMT) [122]