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Merck

Pancreatic stellate cells facilitate pancreatic cancer cell viability and invasion.

Oncology letters (2019-01-25)
Shang-Long Liu, Shou-Gen Cao, Ying Li, Bo Sun, Dong Chen, Dong-Sheng Wang, Yan-Bing Zhou
RESUMO

The biological features of pancreatic cancer and the associated hypoxic environment around the cancer cells often lead to resistance to radiotherapy and chemotherapy. The present study was performed in order to explore the effect pancreatic stellate cells (PSCs) have on the proliferation of pancreatic cancer cells. In the present study, PSCs from human pancreatic cancer tissues were isolated, and the PSCs markers α-smooth muscle actin and desmin were overexpressed in the cytoplasm of PSCs. An MTT assay revealed that PSCs promoted the viability of pancreatic cancer cells. However, the viability of pancreatic cancer cells promoted by PSCs was partially blocked by SB525334. Cellular invasion analysis demonstrated that PSCs promoted the invasion ability of pancreatic cancer cells. An apoptosis assay indicated that PSCs decreased the level of apoptosis induced by gemcitabine. In vivo experiments consisting of mice bearing MIA-PaCa-2 and PSCs demonstrated an increase in the rate of tumor growth compared with MIA-PaCA-2 alone, whereas SB525334 may delay the tumor progression induced by PSCs. The present findings indicated that PSCs promoted the viability and invasion of pancreatic cancer cells, and decreased the apoptosis of pancreatic cancer cells induced by gemcitabine.

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Sigma-Aldrich
Anti-actina monoclonal, α-músculo liso, clone 1A4, purified from hybridoma cell culture
Sigma-Aldrich
Cell Growth Determination Kit, MTT based