How are pancreatic stellate cells activated?

Supernants of cultured human pancreatic cancer cell line SW1990 could stimulate the proliferation of cultured human PSCs, and this stimulation is partly via GAL-3 in the supernants which was expressed and secreted by SW1990 cells. Supernants of cultured human PSCs could stimulate the proliferation and invasion of SW1990 cells, and this was partly related to GAL-3 expressed by cancer cells, because GAL-3 monoclonal antibody could partly inhibit this stimulation. This study, performed by a team led by Professor, Xing-Peng Wang , from Shanghai First People¡¯s Hospital, affiliated with Shanghai Jiaotong University is described in a research article to be published on April 7, 2008 in the World Journal of Gastroenterology.

Pancreatic cancer is one of the most lethal cancers. Difficulty of early diagnosis and resistance to chemotherapy and radiotherapy leads to a low five-year survival rate. New therapeutic targets need to be found for pancreatic cancer treatment.

Previous studies showed GAL-3 was detected in pancreatic cancer tissues, but the role of GAL-3 in the progress of pancreatic cancer was not studied. This in vitro study showed pancreatic cancer cells could stimulate the proliferation of PSCs via GAL-3 and activated PSCs could promote the proliferation and invasion of pancreatic cancer cells partly via the interaction with GAL-3 expressed by cancer cells.

In the view of authors, inhibiting the activation of PSCs and stopping the interaction between pancreatic cancer cells and PSCs provides new hope for controlling pancreatic cancer. GAL-3 could be a new therapeutic target in pancreatic cancer treatment.

GAL-3 was firstly discovered in 1970s. In the late '80s and early '90s, research showed that the expression of GAL-3 was upregulated in cancers of the thyroid, liver, stomach, and tongue. In recent years, research also showed GAL-3 could promote the proliferation, invasion and metastasis of cancer cells.

Further research should be done to elucidate the stimulation mechanism of GAL-3 protein on the proliferation of PSCs, and to explain why the stimulation effect of PSCs on the proliferation and invasion of pancreatic cancer cells is related to GAL-3 expressed bay cancer cells.

Source: World Journal of Gastroenterology