2015PubMedRequires access

Rapamycin inhibits the proliferation of SW1990 pancreatic cancer cell.

Mingjuan Xu, Bu Lm, Kaichun Wu, Lu Lg, Wang Xp

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Abstract

OBJECTIVE: To study the effect of rapamycin on pancreatic cancer cell proliferation, we designed a serial of experiments in human pancreatic cancer cell line SW1990. MATERIALS AND METHODS: SW1990 cells were treated with different concentrations of rapamycin. Cell proliferation was measured by CCK-8 assay and cell colony formation. Cell cycle and apoptosis was analyzed by flow cytometry. The existence of mTOR signaling pathway was demonstrated by immunocytochemistry. Western-blot and real time-PCR were used to test whether mTOR-signaling pathway was inhibited with rapamycin treatment. RESULTS: Our results showed that rapamycin inhibited the cell colony formation and proliferation (p < 0.05). Rapamycin induced G1 cell cycle arrest (p < 0.05) but not cell apoptosis (p > 0.05). p-mTOR, p-p70S6K and p-4E-BP1 were expressed in the cytoplasm of SW1990 cells and those proteins were significantly reduced with rapamycin (p < 0.05). CONCLUSIONS: Rapamycin inhibits SW1990 pancreatic cancer cell proliferation through inhibiting the activation of mTOR pathway.

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OBJECTIVE: To study the effect of rapamycin on pancreatic cancer cell proliferation, we designed a serial of experiments in human pancreatic cancer cell line SW1990. MATERIALS AND METHODS: SW1990 cells were treated with different concentrations of rapamycin. Cell proliferation was measured by CCK-8 assay and cell colony formation. Cell cycle and apoptosis was analyzed by flow cytometry. The existence of mTOR signaling pathway was demonstrated by immunocytochemistry. Western-blot and real time-PCR were used to test whether mTOR-signaling pathway was inhibited with rapamycin treatment. RESULTS: Our results showed that rapamycin inhibited the cell colony formation and proliferation (p < 0.05). Rapamycin induced G1 cell cycle arrest (p < 0.05) but not cell apoptosis (p > 0.05). p-mTOR, p-p70S6K and p-4E-BP1 were expressed in the cytoplasm of SW1990 cells and those proteins were significantly reduced with rapamycin (p < 0.05). CONCLUSIONS: Rapamycin inhibits SW1990 pancreatic cancer cell proliferation through inhibiting the activation of mTOR pathway.

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Available abstract

OBJECTIVE: To study the effect of rapamycin on pancreatic cancer cell proliferation, we designed a serial of experiments in human pancreatic cancer cell line SW1990. MATERIALS AND METHODS: SW1990 cells were treated with different concentrations of rapamycin. Cell proliferation was measured by CCK-8 assay and cell colony formation. Cell cycle and apoptosis was analyzed by flow cytometry. The existence of mTOR signaling pathway was demonstrated by immunocytochemistry. Western-blot and real time-PCR were used to test whether mTOR-signaling pathway was inhibited with rapamycin treatment. RESULTS: Our results showed that rapamycin inhibited the cell colony formation and proliferation (p < 0.05). Rapamycin induced G1 cell cycle arrest (p < 0.05) but not cell apoptosis (p > 0.05). p-mTOR, p-p70S6K and p-4E-BP1 were expressed in the cytoplasm of SW1990 cells and those proteins were significantly reduced with rapamycin (p < 0.05). CONCLUSIONS: Rapamycin inhibits SW1990 pancreatic cancer cell proliferation through inhibiting the activation of mTOR pathway.

Key concepts: PI3K/AKT/mTOR pathway, Cell growth, Cell cycle, Apoptosis, RPTOR, Cancer research, Cell biology, Cell cycle checkpoint

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