Polymorphism of A118G in µ-opioid receptor gene is associated with risk of esophageal squamous cell carcinoma in a Chinese population.

BACKGROUND: Previous studies have indicated a direct effect of µ-opioid receptors on tumor progression or recurrence. An A118G polymorphism in the µ-opioid receptor gene was believed to play an important role in this carcinogenic process. The aim of the present study was to investigate the association between the A118G polymorphism and the risk of esophageal squamous cell carcinoma (ESCC) in a Chinese population. METHOD: The case-control study included 260 cancer patients and 291 controls from a Chinese Han and Chinese TuJia population in Enshi region, China. Genotypes were determined by TaqMan platform. Odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated using multivariate unconditional logistic regression. RESULTS: Compared with the G/G genotype, the A/A genotype exhibited a significantly elevated risk for ESCC (OR = 3.12, 95 % CI [1], 1.11-6.01). A significant interaction between the A118G polymorphism and age, smoking status, and family history of cancer was also found (OR = 2.25, 95 % CI 1.36-4.12; OR = 1.75, 95 % CI 1.23-2.32; OR = 3.14, 95 % CI 1.31-7.28, respectively). CONCLUSION: The A118G polymorphism in the µ-opioid receptor gene might be associated with the risk of ESCC in Chinese population.

[Inhibitory effect of Akt inhibitor deguelin on the growth of PC-3 prostate cancer cells].

OBJECTIVE: To study the inhibitory effect of Akt inhibitor deguelin on PC-3 human prostate cancer cell lines and its possible mechanism. METHODS: PC-3 human prostate cancer cells were cultured in deguelin at the concentrations of 10, 100, 500 and 1 000 nmol/L for 24, 48 and 72 hours, respectively. Then the inhibitory effect of deguelin on the proliferation of the PC-3 cells was determined by MTT assay and that on the cell cycle was detected by flow cytometry. The expression levels of MDM2 and GSK3beta mRNA were measured by RT-PCR and those of MDM2 and GSK3beta proteins by Western blot. RESULTS: At 24, 48 and 72 hours, the inhibition rates of deguelin on the proliferation of the PC-3 prostate cancer cells were (91.10 +/- 3.75), (86.39 +/- 1.16) and (79.51 +/- 2.63)% at 10 nmol/L, (82.46 +/- 3.65), (76.84 +/- 0.97) and (69.69 +/- 2.30) % at 100 nmol/L, (81.46 +/- 0.41), (75.56 +/- 1.12) and (54.07 +/- 3.21)% at 500 nmol/L, and (66.77 +/- 2.82), (58.22 +/- 0.35) and (39.34 +/- 2.40)% at 1000 nmol/L, all with statistically significant differences from the control group (P < 0.01). Deguelin at 10, 100, 500 and 1 000 nmol/L increased the cell cycles blocked in the G0/G1 phase ([62.4 +/- 2.2], [63.6 +/- 1.1 ], [65.0 +/- 0.3] and [66.5 +/- 1.9]%, P < 0.01) and reduced the percentage of the S-phase cells ([14.7 +/- 2.4], [11.1 +/- 5.2], [5.8 +/- 1.1] and [7.0 +/- 0.6]%, P < 0.01). RT-PCR and Western blot showed markedly up-regulated expressions of GSK3 P3 a3beta down-regulated expressions of MDM2 mRNA and proteins in the PC-3 cells treated with deguelin. CONCLUSION: Akt inhibitor deguelin can inhibit the proliferation of PC-3 human prostate cancer cells by affecting the down-stream signal molecules GSK3P3 and betaDM2 in the Akt pathway.

[Prevalence of human papillomavirus in the pubic hair follicles of healthy men and male patients with genital warts].

OBJECTIVE: Human papillomavirus (HPV) commonly exists in healthy individuals, but its prevalence in the pubic hair follicles is not yet clear, nor is the relationship between HPV infection in the pubic hair follicles and the recurrence of genital warts in men. This study aimed to investigate HPV infection in the pubic hair follicles of healthy men and patients with genital warts, and to look into the correlation of HPV infection with recurrent genital warts. METHODS: We included in this study 122 healthy men aged 21-80 years and 86 male patients with genital warts aged 24-61 years, detected HPV in their pubic hair follicles by PCR, and made comparative analysis of the data obtained from the two groups. RESULTS: The positive rate of HPV in the pubic hair follicles of the healthy males was 17.21% (21/122), including 15 cases of HPV6, 4 HPV11, 1 non-HPV6/11 and 1 the mixed type (both HPV6 and HPV11), while that of the genital wart patients was 32.55% (28/86), including 17 cases of HPV6, 7 HPV11, 2 non-HPV6/11 and 2 the mixed type. CONCLUSION: The incidence of HPV infection is higher in patients with genital warts than in healthy men, while the types of HPV involved are basically the same in the two groups, mainly HPV6 and HPV11.

Hypoxia promotes 786-O cells invasiveness and resistance to sorafenib via HIF-2α/COX-2.

Accumulating evidences indicated that hypoxia-induced factors and COX-2 play a important role in tumorigenesis in various human cancer. Yet, the relationship between HIFs and COX-2 in human renal cancer remains unclear. The present study was to examine the role of HIFs and COX-2 in the invasiveness and the resistance to target agent in renal cancer cell line (786-O). In 786-O cells, hypoxia induced the increase in the protein expression of HIF1 and HIF2. We also demonstrate that hypoxia up-regulated the protein expression of COX-2 and Snail, but down-regulation of E-cadherin expression in 786-O cells promoted the invasiveness of 786-O cells and enhanced the resistance of 786-O cells to sorafenib. siRNA target to HIF1α, HIF2α and NS398, a selective inhibitor of COX-2, were used in this study. Only siRNA-HIF2α significantly suppressed the protein expression of HIF2 and COX-2, then decreased the invasive ability and resistance of 786-O cells to sorafenib under hypoxia. NS398 attenuated the increase in invasive cells number and the IC50 value of sorafenib induced by hypoxia. In conclusion, our results demonstrated that hypoxia promoted the invasiveness and resistance of 786-O cells to sorafenib via HIF2 and COX-2 and induced the activation of Snail/E-cadherin, suggesting that a signalling mechanism involving HIF2/COX2 modulates invasiveness and resistance to sorafenib in 786-O cells under hypoxia.