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OBJECTIVE: To probe into the effects of chlorogenic acid (CGA) on proliferation and apoptosis of laryngeal cancer Hep-2 cells through Bcl-2-associated X protein ( Bax ) / B cell lymphoma-2 ( Bcl-2) / cysteinyl aspartate specific proteinase-3 (Caspase-3). METHODS: Laryngeal cancer Hep-2 cells were treated with CGA culture medium of 0, 250, 500, 750 and 1 000 μmol / L for 24 and 48 h respectively to find out the most suitable concentration and treatment time of CGA. Laryngeal cancer Hep-2 cells were divided into the control group (normally cultured laryngeal cancer Hep-2 cells), CGA low concentration group ( 750 μmol / L CGA medium), CGA high concentration group ( 1 000 μmol / L CGA medium ), and CGA high concentration + pathway inhibitor group (1 000 μmol / L CGA medium+50 μmol / L Bax / Bcl-2/ Caspase-3 pathway inhibitor Bax inhibitor peptide V5). Cell counting kit-8 (CCK-8) method was used to determine the proliferation inhibition rate of laryngeal cancer Hep-2 cells in each group, flow cytometry was used to detect the apoptosis rate of laryngeal cancer Hep-2 cells in each group, Western blotting was used to determine the expression of proliferation related protein (ki-67), apoptosis related protein (p53) and Bax / Bcl-2/ Caspase-3 signaling pathway related proteins in laryngeal cancer Hep-2 cells. RESULTS: Compared with the control group, the proliferation inhibition rate, apoptosis rate, p53, Bax and Caspase-3 protein expression levels of laryngeal cancer Hep-2 cells in CGA low and high concentration group were significantly higher, and the ki-67 and Bcl-2 protein expression levels were significantly lower, with statistically significant differences (P< 0. 05); and the proliferation inhibition rate, apoptosis rate, p53, Bax and Caspase-3 protein expression levels of laryngeal cancer Hep-2 cells in CGA high concentration group were higher than those in CGA low concentration group, the of ki-67 and Bcl-2 protein expression levels were lower than those in CGA low concentration group, with statistically significant differences (P < 0. 05). Compared with the CGA high concentration group, the proliferation inhibition rate, apoptosis rate, p53, Bax and Caspase-3 protein expression levels of laryngeal cancer Hep-2 cells in the CGA high concentration+pathway inhibitor group were significantly lower, and the ki-67 and Bcl-2 protein expression levels were significantly higher, with statistically significant differences ( P < 0. 05). CONCLUSIONS: CGA can significantly inhibit the proliferation of laryngeal cancer Hep-2 cells and promote the apoptosis, which may be related to the activation of Bax / Bcl-2/ Caspase-3 signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the effects of apatinib on tumor inhibition rate and tumor cell apoptosis in breast cancer mouse model by regulating extracellular regulated kinase ( ERK) 1 / 2 pathway. METHODS: Human breast cancer cell line MCF-7 cells were inoculated in the right chest wall of nude mice, which were randomly divided into control group, low-dose group[10 mg / (kg·d) of Apatinib] and high-dose group[30 mg / ( kg·d) of Apatinib] after successful modeling, with 12 mice in each group. After intragastric administration once a day for 21 days, the tumor growth curves of three groups were plotted and the tumor inhibition rates were compared. After the last administration, the mice were executed and the tumor tissues were collected, the expression of ERK1 / 2 pathwayrelated proteins [ERK1 / 2, phosphorylated ERK1 / 2(p-ERK1 / 2)] in the tumor tissues was detected by Western blot. The effects of apatinib on MCF-7 cell cycle distribution and cell apoptosis were detected by flow cytometry. RESULTS: After processing with different concentrations of apatinib, the differences in apoptosis rate and the proportion of MCF-7 cells distributed in G0 -G1 phase were statistically significant ( P < 0. 05), among which the apoptosis rate and the proportion of MCF-7 cells distributed in G0 -G1 phase were significantly higher in the group given 20 μmol / L of apatinib than in the other low concentration groups, with statistically significant differences (P<0. 05). The tumor volumes of mice in the high-dose and low-dose groups were significantly lower than that of the control group at the 6th to 21st day of administration, with statistically significant differences (P<0. 05), of which the tumor volumes of mice in the highdose group were the smallest. The mean tumor weights of the high-dose group and low-dose group on the 22nd day were respectively (0. 343±0. 089) g and (0. 658±0. 145) g, which were significantly lower than that of the control group[(1. 163±0. 231) g], with statistically significant differences(P<0. 05). The tumor inhibition rates of the highdose group and low-dose group were respectively 64. 46% and 34. 07%, and there was a dose dependence. The expression levels of ERK1 / 2 and p-ERK1 / 2 in mice in the high-dose group and low-dose group were significantly lower than those in the control group, with statistically significant difference (P<0. 05), of which the expression levels of ERK1 / 2 and p-ERK1 / 2 in mice in the high-dose group were the lowest. CONCLUSIONS: Apatinib can effectively inhibit the ERK1 / 2 signaling pathway in breast cancer cell, induce apoptosis and proliferation of tumor cells, and thus inhibit the growth of tumors in breast cancer mice. [ABSTRACT FROM AUTHOR]