Abstract
To investigate the effects of tetramethypyrazine (TMP) on proliferation and apoptosis of the human gastric carcinoma cell line 7901 and its possible mechanism of action. The viability of TMP-treated 7901 cells was measured with a 3-(4, 5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) and cell apoptosis was analyzed by flow cytometry. The distribution of cells in different phases of cell cycle after exposure of TMPs was analyzed with flow cytometry. To investigate the molecular mechanisms of TMP-mediated apoptosis, the expression of NF-xBp65, cyclinD1 and p16 in SGC-7901 cells was analyzed by reverse transcription- polymerase chain reaction (RT-PCR) and western blotting. TMP inhibited the proliferation of human gastric carcinoma cell line 7901 in dose and time dependent manners. Cell growth was suppressed by TMP at different concentrations (0.25, 0.5, 1.0, 2.0 mg/ml), the inhibition rate is 0.46%, 4.36%, 14.8%, 76.1% (48h) and 15.5%, 18.5%, 41.2%, 89.8% (72h) respectively. When the concentration of TMPs was 2.0mg/ml, G1-phase arrest in the SGC-7901 cells was significant based on the data for cell cycle distribution. RT-PCR demonstrated that NF-xBp65 and cyclin D1 mRNA expression was significantly down-regulated in 7901 cells treated with 2.0 mg/ml TMP for 72h (p<0.05), while the p16 mRNA level was up-regulated (p<0.05). The protein expression of NF-xBp65 and cyclin D1 decreased gradually with the increase in TMP concentration, compared with control cells (p<0.05), while expression of protein p16 was up-regulated (p<0.01). TMP exhibits significant anti-proliferative and pro-apoptotic effects on the human gastric carcinoma cell line SGC-7901. NF-xBp65, cyclinD1 and p16 may also play important roles in the regulation mechanisms.
Highlights
Gastric cancer is the second most common cause of cancer-related death worldwide
We select TMP as our object to observe its effect on the proliferation and apoptosis of human gastric cancer cell line SGC-7901 and determine the expression of NF-κ Bp65, cyclinD1 and p16 to study the mechanism of TMP from the angle of cell cycle and provide a theoretical basis for clinical use of TMP in the treatment of gastric cancer
Growth inhibition of TMP on the SGC-7901 cells The SGC-7901 cells were treated with various concentrations of TMP for 48h and 72h, cell viability was determined by Alamar Blue assay
Summary
Gastric cancer is the second most common cause of cancer-related death worldwide. Some experts have found that TMP has anti-cancer activity and play an active role in the treatment and prevention of lung cancer, stomach cancer, breast cancer and other cancers. They have carried out some explorations on its mechanism, but there is few research and report for the mechanism of TMP on gastric cancer. We select TMP as our object to observe its effect on the proliferation and apoptosis of human gastric cancer cell line SGC-7901 and determine the expression of NF-κ Bp65, cyclinD1 and p16 to study the mechanism of TMP from the angle of cell cycle and provide a theoretical basis for clinical use of TMP in the treatment of gastric cancer
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