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1.
China Occupational Medicine ; (6): 446-448, 2019.
Article in Chinese | WPRIM | ID: wpr-881817

ABSTRACT

OBJECTIVE: To investigate the effect of hyperthermia on the expression of PANDAR, LncRNA-p21 and ST8SIA genes in the human lung adenocarcinoma A549 cells. METHODS: A549 cells were randomly divided into 4 groups. The A549 cells in control group were cultured at 37 ℃; the cells at experimental groups were cultured at 40, 42 or 44 ℃ respectively. The cells in these 4 groups were incubated for 1 hour, and the levels of PANDAR, LncRNA-p21 and ST8SIA genes were analyzed by real-time fluorescence quantitative polymerase chain reaction. RESULTS: In cells cultured at 40, 42 or 44 ℃ experimental groups, the relative expression of PANDAR gene was lower than that of control group(P<0.05). In cells cultured at 44 ℃ experimental group, the relative expression of PANDAR gene was lower than that of the 40 and 42 ℃ experimental groups(P<0.05). There was no significant change in the relative expression of LncRNA-p21 and ST8SIA genes among the four groups(P>0.05). CONCLUSION: Hyperthermia decrease the expression of PANDAR gene in A549 cells.

2.
The Journal of Practical Medicine ; (24): 44-47, 2017.
Article in Chinese | WPRIM | ID: wpr-507079

ABSTRACT

Objective To investigate the expression of miR?126, miR?355 and exportin?5 in lung cancer. Methods The cancer tissue and the tissue adjacent to carcinoma of 47 cases of patients with lung cancer was used to detect the expression of miR?126, miR?355 and Exportin?5 by the real?time fluorescence quantitative PCR. Results Significant difference of the expression of miR?126 (t=2.02,P=0.03) and exportin?5 (t=4.62,P<0.01) was observed in lung cancer tissue and tissue adjacent to carcinoma. Mature miR?126 and pri?miR?126 (R=0.309 , P = 0.044) had a negative correlation in the tissue adjacent to carcinoma. In the cancer tissue,miR?126 and MRP (R=0.432, P=0.019), miR?335 and k167 (R=0.410, P=0.033) were positively correlated, however, exportin?5 and TOPO (R=0.357, P=0.045), the pri?miR?126 and drinking (R=0.340, P=0.024), the pri?miR?126 and MRP (R=0.427, P=0.027) had a negative correlation relationship. Conclusion Expression of miR?126 and exportin?5 was decreased in lung cancer tissue, which may contribute to the occurrence and development of lung cancer.

3.
China Occupational Medicine ; (6): 542-546, 2017.
Article in Chinese | WPRIM | ID: wpr-881636

ABSTRACT

OBJECTIVE: To explore the effect of arsenic on the homeobox D10( HOXD10) gene expression in peripheral blood lymphocytes and human lung adenocarcinoma cell A549. METHODS: ⅰ) A total of 59 workers exposed to arsenic from a arsenic factory were selected as the exposure group and 17 local people without arsenic exposure were chosen as controls by using judgment sampling method. Hydride generation-cold hydrazine trapping-atomic absorption spectrometry was used to detect arsenic levels in urine of these 2 groups. The expression of HOXD10 in peripheral blood lymphocytes was detected by real-time fluorescent quantitative polymerase chain reaction( qRT-PCR).ⅱ) The A549 cells were treated with arsenic trioxide( As_2O_3) with concentration of 0. 0,0. 1,0. 5,1. 0 and 2. 0 μmol/L,and the survival rate of cells was examined by colorimetric assay. The expression of HOXD10 was detected by qRT-PCR. RESULTS: ⅰ) The levels of inorganic arsenic,methylarsonic acid,dimethyl arsenate,total arsenic in the urine,and the relative expression of HOXD10 mRNA in peripheral blood lymphocyte in exposure group were higher than that of the control group( P < 0. 05).ⅱ) As_2O_3 decreased the survival rate of A549 cells in a dose-dependent manner( P < 0. 01) and lead to a dose-dependent increase of HOXD10 mRNA expression( P < 0. 01). A549 cell survival rate and relative expression of HOXD10 mRNA showed a negative correlation,the correlation coefficient was-0. 777( P < 0. 01). CONCLUSION: Arsenic can up-regulate HOXD10 expression in the peripheral blood of occupational arsenic exposure individuals. As_2O_3 can inhibit the proliferation of A549 cells,which may be related to the up-regulation of HOXD10 expression.

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