2005Journal of Qilu OncologyRequires access

Influence of aspirin on proliferation of human lung cancer cells and it mechanism

Guohua Liu

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Abstract

OBJECTIVE: To investigate the influence of aspirin on the proliferation of human lung adenocarcinoma cell line A549 in vitro and its relevant mechanism. METHODS: MTT assay was used to observe the influence of aspirin on the proliferation of A549 cells and immunohistochemistry was used for the expression of COX-2 of A549 cells.Flow cytometry, HE and the TdT-mediated d-UTP nick end-labeling assay (TUNEL) were used to observe the influence of aspirin on the distribution of cell cycle and induction on the apoptosis of A549 cells. RESULTS: Aspirin inhibited A549 cells proliferation in a concentration-and time-dependent manner, and its highest inhibitive rate was 75.6% 72 hours later. After treatment, the expression of COX-2 was markedly reduced.The percentage of cells in G0/G1 phase increased to (60.2±2.33)% and the percentage of cells in S and G2/M phase reduced to (32.9±2.88)% and (6.9±0.66)%,respectively, AI increased from (3.67±1.15)% to (26.33±2.52)% with the raise of aspirin concentration. A549 cells exhibited typical morphologic features of apoptosis by light microscopy. CONCLUSION: Aspirin may inhibit the proliferation of lung adenocarcinoma A549 cells through decreasing COX-2 expression, affecting the distribution of cell cycle and inducing apoptosis.

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OBJECTIVE: To investigate the influence of aspirin on the proliferation of human lung adenocarcinoma cell line A549 in vitro and its relevant mechanism. METHODS: MTT assay was used to observe the influence of aspirin on the proliferation of A549 cells and immunohistochemistry was used for the expression of COX-2 of A549 cells.Flow cytometry, HE and the TdT-mediated d-UTP nick end-labeling assay (TUNEL) were used to observe the influence of aspirin on the distribution of cell cycle and induction on the apoptosis of A549 cells. RESULTS: Aspirin inhibited A549 cells proliferation in a concentration-and time-dependent manner, and its highest inhibitive rate was 75.6% 72 hours later. After treatment, the expression of COX-2 was markedly reduced.The percentage of cells in G0/G1 phase increased to (60.2±2.33)% and the percentage of cells in S and G2/M phase reduced to (32.9±2.88)% and (6.9±0.66)%,respectively, AI increased from (3.67±1.15)% to (26.33±2.52)% with the raise of aspirin concentration. A549 cells exhibited typical morphologic features of apoptosis by light microscopy. CONCLUSION: Aspirin may inhibit the proliferation of lung adenocarcinoma A549 cells through decreasing COX-2 expression, affecting the distribution of cell cycle and inducing apoptosis.

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Available abstract

OBJECTIVE: To investigate the influence of aspirin on the proliferation of human lung adenocarcinoma cell line A549 in vitro and its relevant mechanism. METHODS: MTT assay was used to observe the influence of aspirin on the proliferation of A549 cells and immunohistochemistry was used for the expression of COX-2 of A549 cells.Flow cytometry, HE and the TdT-mediated d-UTP nick end-labeling assay (TUNEL) were used to observe the influence of aspirin on the distribution of cell cycle and induction on the apoptosis of A549 cells. RESULTS: Aspirin inhibited A549 cells proliferation in a concentration-and time-dependent manner, and its highest inhibitive rate was 75.6% 72 hours later. After treatment, the expression of COX-2 was markedly reduced.The percentage of cells in G0/G1 phase increased to (60.2±2.33)% and the percentage of cells in S and G2/M phase reduced to (32.9±2.88)% and (6.9±0.66)%,respectively, AI increased from (3.67±1.15)% to (26.33±2.52)% with the raise of aspirin concentration. A549 cells exhibited typical morphologic features of apoptosis by light microscopy. CONCLUSION: Aspirin may inhibit the proliferation of lung adenocarcinoma A549 cells through decreasing COX-2 expression, affecting the distribution of cell cycle and inducing apoptosis.

Key concepts: A549 cell, Apoptosis, Aspirin, Flow cytometry, Cell cycle, Cell growth, Chemistry, MTT assay

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