Maspin (mammary serine protease inhibitor) is a kind of serpin.Many studies have characterized it as a tumor suppressor based on its ability to inhibit tumor angiogenesis,increase adhesion between tumor cells and ECM,inhibit tumor cell invasion and distant metastasis and promote apoptosis.In recent years,some studies have found maspin expresses high in some cancers,such as in mammary cancer and prostate cancer,while in some other cancers,such as in pancreatic cancer,maspin expression level shows high.The expression levels and biological functions of maspin in different organs still need further study.

Objective To investigate the relationship between the expression level of HOTAIR and cellular radiosensitivity in esophageal squamous cell carcinoma (ESCC). Methods Four ESCC cell lines ( K150, K450, TE-1, and Eca109 ) were used in this study. Quantitative real-time polymerase chain reaction was applied to measure the expression level of HOTAIR in the above cell lines;colony-forming assay was applied to measure the survival fraction of different cells irradiated by different doses of X-ray. The t-test or analysis of variance was applied for analysis of differences. The correlation analysis was used by Pearson methods. Results The four cell lines all showed high expression levels of HOTAIR and radioresistance. Compared with the other three cell lines, Eca109 had a lower expression level of HOTAIR, a lower survival fraction at each radiation dose point, and significantly lower D0 and Dq . The mRNA expression level of HOTAIR and radiosensitivity were K150

Objective To elucidate gene mutation and promoter methylation changes of p16 gene in pheochromocytomas (PHEO) and paragangliomas (PGL) and to assess its relation with tumor clinical characters. Methods A total of 34 tumors (20 PHEO, 14 PG L, 15 benign, 19 malignant) were collected.Direct sequencing of p16 gene after PCR was performed to analyze genetic alterations. Hypermethylation of p16 gene promoter CpG island was analyzed by methylation specific PCR(MSP). In addition, mRNA expression was detected by RT-PCR. Results Homozygous deletion and gene mutation were not observed in 34 PHEO and PGL. Aberrant methylation of p16 gene promoter CpG island was found in 35.3% (12 of 34 tumors, 3 PHEO, 9 PGL). The p16 promoter hypermethylation in PGL was significantly higher than PHEO (P=0. 005). The higher p16 promoter hypermethylation was associated with malignant behavior, tumor number, and younger age at presentation, but no statistical significance, due to the limited number of cases. The p16 mRNA expression in malignant cases was lower than in benign tumors(0.83±0.65 vs 1.12±0.81 ,P=0.278). Conclusion p16 gene homozygous deletion and mutation were not frequent in PHEO and PGL. The promoter hypermethylation is mainly attributed to inactivation of the p16 gene.

Objective To investigate the effect of cisplatin combined with X-ray irradiation on the proliferation of human esophageal squamous cell cancer Eca109 cells and its mechanism. Methods Methyl thiazolyl tetrazolium (MTT) method was used to determine 10％ inhibitory concentration (IC10) and half inhibitory concentration (IC50) of Eca109 cells after 24 h treated with cisplatin in cisplatin group. Then the irradiation group was treated by 4 Gy 6 MV-X ray, cisplatin combined with X-ray irradiation group was treated with 4 Gy 6 MV-X ray irradiation, and IC10 or IC50 cisplatin treatment. After 24 h, 36 h and 48 h of culture, MTT method was used to detect the cell growth and inhibition in each group. Flow cytometry was used to detect cell cycle and apoptosis in each group. Results After 24 h for cisplatin treatment, IC10 and IC50 of Eca109 cells was 0.894 μg/ml and 8.654 μg/ml. After 24 h, 36 h and 48 h of culture, the inhibition rates of 4 Gy+IC10 group were (26.1 ±1.2)％, (56.4 ±4.0)％ and (75.1 ±3.2)％, respectively, and 4 Gy+IC50 group were (55.4±5.9)％, (84.7±3.1)％and (93.8±5.1)％, respectively, and irradiation group were (5.1±2.6)％, (12.2±1.3)％and (37.9±5.3)％, respectively. With the prolonged culture time, the inhibition rates of the three groups were increased gradually, and the differences were statistically significant (all P< 0.01); the inhibition rate of cisplatin combined with X-ray irradiation group was higher than that of irradiation group, and the differences were statistically significant (all P< 0.01). After 48 h of culture, the proportion of G2/M phase cells in the blank control group, irradiation group, 4 Gy+IC10 group, and 4 Gy+IC50 group was increased to (3.0 ±1.5)％, (10.4±0.8)％, (24.8±3.1)％ and (38.9±1.2)％, and the differences were statistically significant (F= 224.3, P<0.001); the proportion of S phase cells in 4 Gy+IC10 group and 4 Gy+IC50 group was (23.4±7.7)％ and (23.2± 5.2)％ respectively, which were lower than that in the blank control group [(44.5 ±2.0)％], and the differences were statistically significant (all P< 0.05). The apoptosis rate of 4 Gy+IC10 group and 4 Gy+IC50 group was (14.0±4.2)％ and (17.9±3.0)％, respectively, which was higher than that of the blank control group [(4.6± 1.8)％], and the differences were statistically significant (all P< 0.05); the apoptosis rate of 4 Gy+IC50 group was also higher than that of irradiation group [(7.1±0.9)％], and the difference was statistically significant (P=0.001). Conclusions Cisplatin combined with X-ray irradiation can significantly inhibit the proliferation of human esophageal squamous cell cancer Eca109 cells in a dose and time-dependent manner. The main mechanism may be related with the fact that low-dose or high-dose cisplatin and X-ray irradiation makes the Eca109 cells arrest at G2/M phase, so that the sensitivity of cells to irradiation can be increased.