Objective:To investigate the effects of fibroblast growth factor receptor 1(FGFR1)on the resistance of colorectal cancer(CRC)cells to oxaliplatin(OXA).Methods:An OXA-resistant cell line(HCT8/OXA)was established by treating HCT8 CRC cells with low-dose OXA for a long period in vitro.The CCK-8 assay was used to compare the viability of the HCT8 and HCT8/OXA cells after OXA treatment and to exam-ine their resistance to the anticancer drug.Second-generation high-throughput sequencing technology was used to identify differentially ex-pressed genes between the parental and drug-resistant cells.The expression of FGFR1 in the HCT8 and HCT8/OXA cells was detected by Western blot assay.Colony formation and flow cytometric assays were used to determine cell proliferation and apoptosis,respectively.The expression of PI3K/AKT signaling pathway-related proteins was detected using Western blot assay.Results:Compared with the levels in the HCT8 cells,the FGFR1 levels were significantly increased in the HCT8/OXA cells(P<0.01).FGFR1 overexpression in the HCT8 cells increased their drug resistance(P<0.01)and proliferation(NC+OXA:236.67±6.24;FGFR1+OXA:568.33±6.24)and decreased their apoptotic rate after OXA treatment(NC+OXA:27.83±0.85;FGFR1+OXA:17.47±1.25).FGFR1 knockdown in the HCT8/OXA cells reduced their drug resistance(P<0.01)and proliferative ability(Si-NC+OXA:411±8.29;Si-FGFR1+OXA:233.33±20.55)and increased their apoptotic rate(Si-NC+OXA:2.85±0.17;Si-FGFR1+OXA:14.42±0.77).FGFR1 inhibited the activity of the PI3K/AKT signaling pathway and cell apoptosis and improved the proliferation and drug resistance of the CRC cells.By contrast,an activator of the PI3K/AKT pathway blocked the effects of FGFR1 on this sig-naling pathway and drug resistance in the CRC cells.Conclusions:FGFR1 can inhibit the PI3K/AKT signaling pathway and thereby reduce the sensitivity of CRC cells to OXA.

Objective:To investigate the effects of fibroblast growth factor receptor 1(FGFR1)on the resistance of colorectal cancer(CRC)cells to oxaliplatin(OXA).Methods:An OXA-resistant cell line(HCT8/OXA)was established by treating HCT8 CRC cells with low-dose OXA for a long period in vitro.The CCK-8 assay was used to compare the viability of the HCT8 and HCT8/OXA cells after OXA treatment and to exam-ine their resistance to the anticancer drug.Second-generation high-throughput sequencing technology was used to identify differentially ex-pressed genes between the parental and drug-resistant cells.The expression of FGFR1 in the HCT8 and HCT8/OXA cells was detected by Western blot assay.Colony formation and flow cytometric assays were used to determine cell proliferation and apoptosis,respectively.The expression of PI3K/AKT signaling pathway-related proteins was detected using Western blot assay.Results:Compared with the levels in the HCT8 cells,the FGFR1 levels were significantly increased in the HCT8/OXA cells(P<0.01).FGFR1 overexpression in the HCT8 cells increased their drug resistance(P<0.01)and proliferation(NC+OXA:236.67±6.24;FGFR1+OXA:568.33±6.24)and decreased their apoptotic rate after OXA treatment(NC+OXA:27.83±0.85;FGFR1+OXA:17.47±1.25).FGFR1 knockdown in the HCT8/OXA cells reduced their drug resistance(P<0.01)and proliferative ability(Si-NC+OXA:411±8.29;Si-FGFR1+OXA:233.33±20.55)and increased their apoptotic rate(Si-NC+OXA:2.85±0.17;Si-FGFR1+OXA:14.42±0.77).FGFR1 inhibited the activity of the PI3K/AKT signaling pathway and cell apoptosis and improved the proliferation and drug resistance of the CRC cells.By contrast,an activator of the PI3K/AKT pathway blocked the effects of FGFR1 on this sig-naling pathway and drug resistance in the CRC cells.Conclusions:FGFR1 can inhibit the PI3K/AKT signaling pathway and thereby reduce the sensitivity of CRC cells to OXA.

Objective To explore the effects of different dose rates of X-ray under the same dose on cell clonogenic formation in non-small-cell lung cancer cell line A549 in order to provide experimental basis for clinical radiotherapy plan. Methods The A549 cells were cultured at low density and irradiated with X-rays at dose of 4 Gy and selected dose rates of 1, 2, 4 and 6 Gy/min, respectively, from a linear accelerator. The 8th day after irradiation, the cells were fixed and stained with Giemsa solution, and colonies containing at least 50 cells were counted. The plating efficiency and surviving fraction were calculated. Results The clonogenic number in non-irradiated cells was 88.6±4.6. The numbers were significantly reduced in irradiated cells at dose rate 1, 2, 4 and 6 Gy/min (12.3±3.4, 9.0±0.8, 5.6±1.0, 11.5±1.7, respectively) than that in non-irradiated control cells (F=678.799, P<0.05). The plating efficiencies were decreased in irradiated cells, especially in 4 Gy/min irradiated cells, which was lower than that in any of the other three dose rate groups (P< 0.05). Conclusions Though at same radiation dose, cancer cells have different clonogenic formation efficiency when irradiation with X-ray at different dose rates. Thus, treatment with optimal dose rate may improve the radiotherapy efficacy.