Search

Objective: To investigate the influence of aerosols on the expression of cyclin B(1), cyclin C and proliferating cell nuclear antigen (PCNA) in wound tissue healing of burned rat models., Methods: Sprague Dawley (SD) rats were inflicted as the deep partial thickness burn models. Rats were randomly divided into experimental group and control group. The experimental group were treated with aerosols. Samples were collected in 1 approximately 10 postburn days. Immunohistochemistry and image analysis methods were conducted to examine the expression of cyclin B(1), cyclin C and PCNA in both experimental and control groups., Results: The expression of cyclin C in experimental group was detected in nucleus of skin basal cell on the second postburn day, increased evidently at the fifth days and sustained at high expression level up to the tenth days after treatment. The expression of cyclin C in experimental group was significantly higher than control group (P < 0.05). The expression of PCNA was first observed in skin basal cell nucleus and hair follicle cell nucleus in both experimental and control group on the third postburn day. The expression of PCNA increased evidently at the fifth days in experimental after treatment and that increased evidently at the seventh days in control group, which showed there were lots of active proliferation cell. And the difference of the expression of PCNA between experimental and control group was significant (P < 0.01). The expression of cyclin B(1) was detected in nucleus and cytoplasm of skin basal cell in both groups on the third postburn day, and no difference between the experimental and control group (P > 0.05)., Conclusions: Aerosols can up-regulate the expression of cyclin C and PCNA in skin basal cell nucleus. Therefore the aerosols can accelerate wound tissue healing.

Objective: To investigate the relation between the expression of cyclin B1 and multidrug resistance in adult patients with acute leukemia., Methods: The proteins expression of cyclin B1, p170 was measured with flow cytometric analysis in 85 adult de novo acute leukemia patients (AL) and 17 normal control (NC). The expression of cyclin B1, multidrug resistance gene (mdr-1), topoisomerase IIalpha, beta (TOPOIIalpha, beta) and bcl-2 mRNA in these patients was measured with semi-quantify reverse transcription polymerase chain reaction (RT-PCR)., Results: (1) The expression of cyclin B1 protein (M = 12.3%) and mRNA (M = 0.217) in the treatment resistance group was significantly lower than the sensitive group cyclin B1 protein (M = 22.7%) and mRNA (M = 0.563) (P < 0.05), so was the mRNA of TOPOIIalpha (M = 0.236), TOPOIIbeta (M = 0.328) than the sensitive group TOPOIIalpha (M = 0.514), TOPOIIbeta (M = 0.635) (P < 0.01). Cyclin B1 protein expression was lower than 5% and there were no expression of cyclin B1, TOPOIIalpha, mdr-1 mRNA in the NC group under the same condition. (2) The p170 protein (M = 14.3%) and mdr-1 (M = 1.071), bcl-2 (M = 0.941) mRNA expression in the resistant group was significant higher than the sensitive group p170 protein (M = 3.6%) and mdr-1 (M = 0.094), bcl-2 (M = 0.153) (P < 0.01). (3) The expression of cyclin B1 protein and TOPOIIalpha, TOPOIIbeta mRNA was positive correlated (r(TOPOIIalpha) = 0.472, P < 0.01; r(TOPOIIbeta) = 0.683, P < 0.01), so was the cyclin B1 mRNA (r(TOPOIIalpha) = 0.319, P < 0.05; r(TOPOIIbeta) = 0.527, P < 0.05). (4) There was no correlation between cyclin B1 and p170, mdr-1, bcl-2. (5) By Binary logistic forward conditional analysis we concluded that cyclin B1 correlated with atypital mutidrug resistance., Conclusions: Low expression of cyclin B1 might be a unfavorable prognostic factor for patients with AL and measurement of both cyclin B1 and TOPOIIalpha, TOPOIIbeta gene expression would predict drug resistance in adult acute leukemia patients.

Aim: To investigate the radiosensitizing effect and mechanism of action of staurosporine (STP) in human colon carcinoma HT-29 and breast cancer MCF-7/ADR cells., Methods: The effect of STP on the cytotoxicity of X-ray was determined by clonogenic assay. The effect of STP on cell cycle arrest induced by X irradiation was studied in two cell lines by using flow cytometry, Western Blotting was performed to indicate the changes of cyclin B1 and cdc2 protein levels., Results: STP sensitized the two cell lines to X-ray by clonogenic assay. STP potentiated the cytotoxicity of X-ray by 2.10- and 2.09-fold in HT-29 and MCF-7/ADR cells. Flow cytometry assay showed that exposure of HT-29 and MCF-7/ADR cells to X-ray caused cells arrest in G2 phase. The percentage of arrest G2 phase cells were 56% and 52.7%, respectively. The addition of STP after irradiation resulted in a dose-dependent reduction of G2 phase arrest induced by X-ray. Furthermore, the results showed that STP blocked decrease of cyclin B1 expression induced by X-ray, while mitotic index measurement indicated that X-ray-irradiated cells treated with STP entered mitosis. The data suggested that the potentiation of cytotoxicity of X-ray by STP is associated with the suppression of cyclin B1 expression, which result in the abrogation of G2 arrest, before the cells entered into M phase, they had not enough time to repair., Conclusion: STP is a potent G2 checkpoint abrogator and markedly enhanced the cytotoxicity of X irradiation in the p53 mutant cancer cells.

Objective: To confirm the unscheduled in vivo and in vitro expression models of cyclin B1 in cancer cells so as to study the different profiles of cyclin B1 in G(1)-phase immortal cells under different culture states and culture conditions., Methods: Multiparameter flow cytometry (FCM) was used to correlate the expression of cyclin B1 with the position in cell cycle of immortal cells in vivo and in vitro using the MOLT-4 cell line as control. Cells which belonged to G(1)-phase were sorted by FCM according DNA diploidy, and then the expression of cyclin B1 was examined by confocal microscope to confirm the results. For further analysis, different subgroups in G(1) phase were sorted according to the fluorescent intensity of cyclin E, and then the exact period in G(1) phase when cyclin B1 was expressed, were assayed by Western blot., Results: Unscheduled expression of cyclin B1 expressed in G(1)-phase was found not only in synchronized leukemia cells MOLT-4 and in vivo transformed T-7 cells, but also in vivo tumor cells detached from clinical samples. In the synchronized growing cells, cyclin B1 was mainly detected in the early G(1) phase, while in transformed T7 cells, cyclin B1 was mainly detected in the late G(1) phase., Conclusion: The limitation of detecting cyclin B1 is due to its unscheduled expression, rending cyclin B1 being detected at different time-spots in the G(1) phase. This phenomenon may be related to the adjustment between the loss of control in cell proliferation and cell apoptosis, thereby leading to tumorigenesis.