Detection of human cyclin C gene expression in childhood acute lymphocytic leukemia using real-time fluorescence quantitative PCR / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the relationship between human cyclin C (CCNC) gene and childhood acute lymphocytic leukemia (ALL).</p><p><b>METHODS</b>The total RNA isolated from myeloid tissues of normal children and of children with newly diagnosed ALL and from ALL cell line 6T-CEM was reversely transcribed into cDNA. Real-time fluorescence quantitative PCR method was used to detect CCNC gene expression.</p><p><b>RESULTS</b>CCNC was expressed in myeloid tissues of normal children and of children with newly diagnosed ALL as well as 6T-CEM. The relative expression level of CCNC gene in children with newly diagnosed ALL was significantly lower than in normal controls (2.35 +/- 0.83 vs 13.5 +/- 0.30; P <0.05).</p><p><b>CONCLUSIONS</b>CCNC gene shows lower expression in children with newly diagnosed ALL, suggesting that it may be a tumor suppressing gene in childhood ALL.</p>

Influence of aerosols on the expression of cyclin B1, cyclin C and proliferating cell nuclear antigen in wound tissue healing of burned rat models / 中华外科杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSIONS</b>Aerosols can up-regulate the expression of cyclin C and PCNA in skin basal cell nucleus. Therefore the aerosols can accelerate wound tissue healing.</p>

Expression of G1 cell cycle related genes in triamcinolone acetonide treated keloid fibroblasts

The effect of triamcinolone acetonide(TA) on the expression of Gl related genes was investigated the cultured keloid fibroblast. The addition of TA to the culture medium resulted in growth inhibition of keloid fibroblast. TA reduced the expression of cyclin A, B, E and cyclin dependent kinase(CDK) 2 mRNA, but unexpectedly, the expression of cyclin C, Dl and CDK4 mRAN was not affected significantly as compared with those of normal fibroblast. Expressions of p16, p21 and p27, the wellestabilished CDK-inhibitors, were also investigated. The level of p16 was not detected in both normal and keloid fibroblasts and the expression of p27 was significantly decreased in keloid fibroblast. The expression of p21 was dramatically increased in keloid fibroblast but not significantly changed in normal fibroblast. Also the expressions of p53 and pRb, the well known tumor suppressor genes, were increased by the addition of TA. These data suggested that the observed growth inhibitory effect of TA may be related to transcriptional inactivation of cyclin A, B, E and CDK2 and to the transcriptional activation of p21, but the mechanisms of unchanged expression of cyclin C, Dl and CDK4 mRNA remain to be elucidated.

Expression of Cell Cycle Related Genes in HL60 Cells Undergoing Apoptosis by X-irradiation / 대한방사선종양학회지

PURPOSE: To evaluate changes in expression of cell cycle related genes during apoptosis induced in HL60 cells by X-irradiation to understand molecular biologic aspects in mechanism of radiation therapy. MATERIAL AND METHODS: HL-60 cell line (promyelocytic leukemia cell line) was grown in culture media and irradiated with 8 Gy by linear accelerator (6 MV X-ray). At various times after irradiation, ranging from 3 to 48 hours were analyzed apoptotic DNA fragmentation assay for apoptosis and by western blot analysis and semi-quantitative RT-PCR for expression of cell cycle related genes (cyclin A, cyclin B, cyclin C, cyclin D1, cyclin E, cdc2, CDK2, CDK4, p16INK4a, p21WAF1, p27KIP1, E2F, PCNA and Rb). RESULTS: X-irradiation (8 Gy) induced apoptosis in HL-60 cell line. Cycline A protein increased after reaching its peak 48 h after radiation delivery and cyclin E, E2F, CDK2 and RB protein increased then decreased after radiation. Radiation induced up-regulation of the expression of E2F is due to mostly increase of phosphorylated retinoblastoma proteins (ppRb). Cyclin D1, PCNA, CDC2, CDK4 and p16INK4a protein underwent no significant change at any times after irradiation. There was not detected p21WAF1 and p27KIP1 protein. Cyclin A, B, C mRNA decreased immediately after radiation and then increased at 12 h after radiation. Cyclin D1 mRNA increased immediately and then decreased at 48 h after radiation. After radiation, cyclin E mRNA decreased with the lapse of time. CDK2 mRNA decreased at 3 h and increased at 6h after radiation. CDK4 mRNA rapidly increased at 6 to 12 h after radiation. There was no change of expression of p16INK4a and not detected in expressin of p21WAF1 and p27KIP1 mRNA. CONCLUSION: We suggest that entry into S phase may contribute to apoptosis of HL60 cells induced by irradiation. Increase of ppRb and decrease of pRb protein are related with radiation induced apoptosis of HL60 cells and tosis of HL60 cells induced by irradiation. Increase of ppRb and decrease of pRb protein are related with radiation induced apoptosis of HL60 cells and this may be associated with induction of E2F and cyclinE/CDK2. These results support that p21WAF1 and p27KIP1 are not related with radiation induced-apoptosis.