Relationship between cyclin G1 and human papilloma virus infection in cervical intraepithelial neoplasia and cervical carcinoma / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To evaluate the overexpression of cyclin G1 in cervical intraepithelial neoplasia (CIN) and cervical carcinoma, and the correlation between cyclin G1 and high-risk human papilloma virus (HPV) infection.</p><p><b>METHODS</b>All of the specimens were obtained from the Department of Pathology of China-Japan Friendship Hospital from January 2000 to August 2004. We detected the expression of cyclin G1 with immunohistochemistry, HPV16/18 infection with in situ hybridization, and high-risk HPV infection with Hybrid capture system II (HC-II) in normal group (25 cases), CIN I (48 cases), CIN II (56 cases), CIN III (54 cases), and invasive cervical squamous-cell carcinoma (SCC, 31 cases).</p><p><b>RESULTS</b>The positive rates of cyclin G1 expression in CIN (77.85%) and SCC cervical tissues (87.10%) were significantly higher than normal (8.00%, P < 0.01), and the intensities of cyclin G1 expression in CIN (40.60%) and SCC cervical tissues (61.51%) were significantly higher than normal (2.72%, P < 0.05). The positive rates and intensities of cyclin G1 expression increased gradually with the grade of cervical lesions. High-risk HPV infection rates were higher in CIN and SCC than normal groups (P < 0.05). There was a positive correlation between cyclin G1 expression and high-risk HPV infection detected with HC-II (Kendall's tau-b = 0.316, 0.269, 0.352, and 0.474 in CIN I, CINII, CIN III, and SCC, respectively, P < 0.05).</p><p><b>CONCLUSIONS</b>Cyclin G1 is overexpressed in CIN and SCC. Cyclin G1 may be a biomarker for detecting CIN and SCC. Cyclin G1 may play an important role in the oncogenesis of CIN and SCC by high-risk HPV infection.</p>

Proliferation regulation effect of cyclin G1 antisense oligodeoxy-nucleotides with liposomal transfection on HL-60 cell / 中国实验血液学杂志

To investigate the effect of cyclin G1 antisense oligodeoxynucleotide (ASON) with liposomal transfection on mediating proliferation of HL-60 cell, the cyclin G1 ASON with liposomal transfection was used in vitro in co-culture with HL-60 cell, the protein and mRNA expression levels of cyclin G1 were measured by immunocytochemistry assay and RT-PCR. The cell apoptosis was detected by electron microscopy, in situ cell apoptosis detection kit (POD), DNA gel electrophoresis and flow cytometry (FCM). The results showed that in the cyclin G1 ASON group the protein and mRNA expression of cyclin G1 were significantly inhibited as compared with sense oligodeoxynucleotide (SON) group and blank group. When the ASON concentration increased, the proliferation ratio of HL-60 cell and CFU of HL-60 were also significantly inhibited. There was apoptosis of HL-60 cell. In conclusion, cyclin G1 ASON can specifically inhibit its protein and mRNA expression levels as well as the HL-60 cell proliferations and can accelerate the apoptosis of leukemia cells with concentration-dependent effect of ASON.

Anti-tumor Effects of Epigallocatechin-3-gallate Extracted from Green Tea on Ovarian Cancer Cell Lines / 대한산부인과학회잡지

OBJECTIVE: A constituent of green tea, (-)-epigallocatechin-3-gallate (EGCG), has been known to possess anti-diabetes, anti-hypertension and anti-cancer properties. In this study, we investigated the anticancer effects of EGCG on human ovarian cancer cell lines. The growth inhibitory mechanism(s) and regulation of cell cycle-related proteins by EGCG were also evaluated. METHODS: To carry out cell counting assay to observe the anti-proliferative effects, we treated 25, 50, and 100 uM EGCG to both ovarian cancer cell lines SKOV-3 and OVCAR-3, respectively. Also, we treated EGCG to PA-1 cells with 6.25, 12.5 and 25 uM, respectively. Six days later, we examined the characteristics of apoptosis and changes in cell cycle regulation by cell counting assay, Annexin V-FITC staining and DNA fragmentation assay, and FACS analysis. In addition, protein and gene expression patterns in SKOV-3 cell were investigated by using cell cycle cDNA chip, RT-PCR, and Western blot analyses. RESULTS: Inhibition of cell growth by cell counts showed in SKOV-3 cells with 48.8%, 82.5%, 99.2% after six days of the treatment with 25, 50, 100 uM of EGCG, respectively. OVCAR-3 cells showed 53.9%, 84.8%, and 97.7% growth inhibition patterns. And PA-1 cells showed 17.1%, 48.4%, and 74.1%, as compared to control. When SKOV-3 cells were tested for EGCG-induced apoptosis, apoptotic cells were observed with 8.6, 11.4, and 23.3-fold at 25, 50, 100 uM EGCG, respectively. And PA-1 cells showed 1.7, 2.4, and 4.2-fold, as compared to control. In contrast, OVCAR-3 did not show EGCG-induced apoptosis. When SKOV-3 cells were tested for their gene expression using cell cycle cDNA chip after treatment with 24.5 uM of EGCG, up-regulations of p21, Bax and cyclin G were shown, while down-regulations of CDK6, E2F-4, and cyclin A were shown. In Western blot assay, up-regulations of Bax and p21 proteins were shown, while down- regulations of cyclin D1, Bcl-XL, Rb, CDK2, E2F-1, E2F-4, PCNA proteins were shown. CONCLUSION: These data support that EGCG can inhibit ovarian cancer cell growth through induction of apoptosis and cell cycle arrest as well as regulation of gene and protein expressions. Thus, EGCG likely provides an additional option for a new and potential drug approach for ovarian cancer.

Effect of cyclin G1 antisense oligodeoxynucleotides (ASON) on the growth of HL-60 cells in nude mice / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the inhibition effect of cyclin G(1) antisense oligodeoxynucleotides (ASON) on the growth of HL-60 cells in nude mice.</p><p><b>METHODS</b>(1) Nude mice were divided into control group, sense oligodeoxynucleotides (SON) group and ASON group. After (60)Co radiation, with HL-60 cells SON group and ASON group were subcutaneously innoculated; (2) The weight and volume of tumors were continually measured; (3) The morphology of tumor cells was observed by microscope; (4) The protein and mRNA expression levels of cyclin G(1) were determined by flow cytometry (FCM) and reverse transcription polymerase chain reaction (RT-PCR); (5) The cell apoptosis was detected by electron microscopy and FCM.</p><p><b>RESULTS</b>(1) The inhibition rate of tumor in ASON group was 69.4%. In ASON group, the wight and volume of tumor were significantly lower than those in SON group and control group. (2) The HL-60 cells in ASON group showed morphologically smaller nuclei, less mitosis, less heteromorphosis and apoptosis.</p><p><b>CONCLUSION</b>The cyclin G(1) ASON can inhibit the growth of HL-60 cells in nude mice and induce apoptosis.</p>