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In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adcnocarcinoma were established.When the largest diameter of tumor reached 1.0 cm,all nude mice were randomly divided into 4 groups: Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest diameter and the vertical diameter of tumor were measured at different time points.At the 16th day,mice were executed,and the tumors were applied to analysis of rate of tumor cell apoptosis,and the expression levels of basic fibroblast growth factor(bFGF)mRNA were detected by reverse transcription-polymerase chain reaction(RT-PCR)and those of vascular endothelial growth factor(VEGF)by immunohistochemistry.The results demonstrated that the rate of tumor inhibition in combined treatment group was higher than that in other groups.And the rate of tumor cell apoptosis in combined treatment group was also higher than that in other groups.Meanwhile,the levels of bFGF mRNA and VEGF expression in combined treatment group were lower than those in other groups.It was concluded that Endostar obviously enhanced the curative effectiveness of radiotherapy on lung adenocarcinoma A549 in mice.The underlying mechanisms may involve the down-regulation of bFGF mRNA and VEGF expression to inhibit angiogenesis by Endostar and the cooperative effect of Endostar and radiotherapy to synergistically promote tumor cell apoptosis.And Endostar inhibits angiogenesis by down-regulating the expression of bFGF mRNA and VEGF.
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This study examined the role of PI3K/Akt pathway in radiosensitization of DNA damage of cervical carcinoma cells.The 50% inhibition concentration(IC50)of cisplatin and docetaxel in HeLa cells was detected by Mono-nuclear cell direct cytotoxicity assay(MTT)in vitro.HeLa cells were treated by cisplatin/docetaxel of 10 percent of IC20 alone or combined with LY294002 for 24 h,and then radiated by different doses of X-ray.The cell survival ratio was obtained by means of clone formation.One-hit multi-target model was fitted to the cell survival curve to calculate dose quasithreshold (Dq),mean lethal dose(D0),2Gy survival fraction(SF2)and sensitization enhancement ratio(SER).The pAkt and total Akt expression was detected by Western blotting and DNA damage by neutro-comet electrophoresis.The HeLa cells were randomly divided into 7 groups in terms of different treatments: Control; radiation treatment(RT)group; LY294002+RT group; cisplatin+RT group; docetaxel+RT group; LY294002+cisplatin+RT group; LY294002+docetaxel+RT group.The apoptosis ratio of each group was measured by flow cytometry.The results showed that docetaxel and cisplatin significantly enhanced the phosphorylation of Akt in radiation-treated HeLa cells.The Dq,Do and SF2 in LY294002-contained groups were lower than those in docetaxel or cisplatin+RT group.The SER in the LY294002+docetaxel+RT group was 1.35 times that of the docetaxel+RT group,and that in the LY294002+cisplatin+RT group 1.26 times that of the cisplatin+RT group.The Comet electrophoresis showed that tail distance in the LY294002+cisplatin+RT group or LY294002+do-cetaxel+RT group was longer than in the cisplatin+RT group or docetaxel+RT group.The apoptosis ratio in the LY294002+cisplatin+RT group or LY294002+docetaxel+RT group was higher than in the cisplatin+RT group or docetaxel+RT group.It was concluded that inhibiting PI3K/Akt pathway can increase the effect of docetaxel and cisplatin on the radiosensitivity of HeLa cells and DNA damage resulted from radiation.
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ex-pression in breast cancer cells with high ERBB2 expression. It was concluded that radiation could induce ERBB2 nuclear transport, and nuclear ERBB2 may correlate with radiation resistance in breast cancer cells with high ERBB2 expression.
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The effect of astrocytes on the growth and differentiation of co-cultured mesenchymal stem cells (MSCs) was studied. MSCs of Wistar rats were isolated, cultured and labeled with Hoechst33342. The labeled MSCs were co-cultured with astrocytes in DMEM/F12/10%FBS. The growth status and morphologic change of MSCs were observed. The expression of specific protein NeuN, GFAP and CNP was detected by using immunofluorescence staining. The results showed that the two kinds of co-cultured cells grew well. Some labeled MSCs stretched out long processes with spin, triangle and star shapes. Immunofluorescence stain showed that these cells expressed NeuN, GFAP or CNP. It was suggested that astrocytes could promote the prolifevation of co-cultured MSCs and induce them to differentiate into neural like cells.
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The correlation between aquaporin 1 (AQP1) and hypoxia-inducible factor 1 (HIF 1) in breast cancer tissues was preliminarily studied. In 155 cases of breast cancer, the expression levels of AQP1 were detected by immunohistochemisty in HIF1-positive group or HIF1-negative group, and the correlation between AQP1 and HIF1 was analyzed. The overexpression of AQP1 and HIF1 were observed in 155 cases of breast cancer tissues. The expression level of AQP1 in HIF1-positive group was significantly higher than that in HIF1-negative group. The positive expression rate of AQP1 was 296.55±24.67 and 168.37±37.53 in HIF1-positive group and HIF1-negative group respectively with the difference being very significant between them (P<0.001). It was concluded that AQP1 was overexpressed in the HIF1-positive group and there were some correlations between AQP1 and HIF1, suggesting they interact each other and regulate the oncogenesis of breast cancer.