Objective To investigate the role of pancreatic stellate cells (PSCs) and galectin-3 (GAL-3) on the proliferation and infiltration of pancreatic cancer cell line SW1990. Methods Human pancreatic cancer cell line SW199...Objective To investigate the role of pancreatic stellate cells (PSCs) and galectin-3 (GAL-3) on the proliferation and infiltration of pancreatic cancer cell line SW1990. Methods Human pancreatic cancer cell line SW1990 and PSCs were cultured in vitro. Supernatant of cultured PSCs and SW1990 cells was collected. Expressions of GAL-3 in SW1990 cells and PSCs were detected by ELISA, RT-PCR and Western blot. The proliferation of those cultured PSCs and SW1990 cells were measured by MTT assay and flowcytometry. Infiltration of SW1990 cells was detected by cell infiltration kit. Results SW1990 cells expressed GAL-3 and the expression was up-regulated by the supernatant fluid of cultured PSCs. PSCs did not express GAL-3. SW1990 cells could stimulate the proliferation of PSCs via GAL-3. GAL-3 antibody could inhibit SW1990 cells proliferation and infiltration, which indicated that supernatant of PSCs might stimulate the proliferation of SW1990 cells through the interaction with GAL-3 protein. The supernatant fluid of PSCs could enhance the invasiveness of SW1990 cells through the interaction with GAL-3. Conclusion GAL-3 and PSCs was involved in the proliferation and infiltration process of pancreatic cancer.展开更多
文摘Objective To investigate the role of pancreatic stellate cells (PSCs) and galectin-3 (GAL-3) on the proliferation and infiltration of pancreatic cancer cell line SW1990. Methods Human pancreatic cancer cell line SW1990 and PSCs were cultured in vitro. Supernatant of cultured PSCs and SW1990 cells was collected. Expressions of GAL-3 in SW1990 cells and PSCs were detected by ELISA, RT-PCR and Western blot. The proliferation of those cultured PSCs and SW1990 cells were measured by MTT assay and flowcytometry. Infiltration of SW1990 cells was detected by cell infiltration kit. Results SW1990 cells expressed GAL-3 and the expression was up-regulated by the supernatant fluid of cultured PSCs. PSCs did not express GAL-3. SW1990 cells could stimulate the proliferation of PSCs via GAL-3. GAL-3 antibody could inhibit SW1990 cells proliferation and infiltration, which indicated that supernatant of PSCs might stimulate the proliferation of SW1990 cells through the interaction with GAL-3 protein. The supernatant fluid of PSCs could enhance the invasiveness of SW1990 cells through the interaction with GAL-3. Conclusion GAL-3 and PSCs was involved in the proliferation and infiltration process of pancreatic cancer.
