Objective To study the relationship between CDC25A (cell division cycle 25A) expression and the development of gastric adenocarcinoma. hTe effect of artesunate (Art) on CDC25A and gastric cancer cells were also investigated.Methods hTe CDC25A protein expression in gastric adenocarcinoma was detected by lfow cytometry assay. SGC-7901 cells were divided into four groups: control group and 30, 60, 120μmol/L Art groups. Cell apoptosis, cell cycle and CDC25A protein expression in SGC-7901 cells were determined by lfow cytometry atfer the treatment of different concentrations of Art (30, 60, 120μmol/L) for 24h, while the same volume of saline was used in the control.Results CDC25A protein expression level in gastric adenocarcinoma (419.69±21.91) was signiifcantly higher than that in normal gastric tissues (316.11±24.23,P<0.01). hTe cell apoptosis rates of 30, 60, 120μmol/L Art groups (5.48%±0.67%, 12.55%±1.17%, 23.43%±2.18%) were significantly higher than that of control group (0.87%±0.14 %,P<0.05), with an Art dose dependent manner. hTe cell proliferation indices of 30, 60, 120μmol/L Art groups (39.18%±0.53%, 35.71%±0.99%, 31.73%±1.02%) were signiifcantly lower than that of control group (44.12%±2.51%,P<0.01). hTe CDC25A protein expression levels of 30, 60, 120μmol/L Art groups (414.80±4.06, 397.86±3.61, 345.68±7.11) were significantly lower than that of control group (433.99±1.56,P<0.01).ConclusionhTe abnormally increased expression level of CDC25A may be involved in the development of gastric adenocarcinoma. Art can inhibit the growth of SGC-7901 cells by down-regulating the expression of CDC25A protein.

Objective: To investigate the expression of ciRS-7 in esophageal squamous cell carcinoma (ESCC) and its effect on the cellular proliferation, migration and invasion. Methods: The cancer tissues and paired adjacent normal tissues from 60 ESCC patients treated in the Fourth Hospital of Hebei Medical University between May, 2016 andApril, 2017 were selected for this study. The expressions of ciRS-7 were detected by qRT-PCR. After over-expressing or silencing of ciRS-7, the proliferation of ESCC cell line TE1 was measured by CCK-8 assay; and the migration and invasion were tested by wound healing assay and Transwell invasion assay，respectively. Finally, the effect was validated via animal experiment. Results: CiRS-7 was highly expressed in ESCC tissues (P<0.05), and its expression level was closely related to pathological grade and lymph node metastasis (P<0.05). Over-expression of ciRS-7 significantly increased the proliferation, migration and invasion (all P<0.05) of TE1 cells; while silencing of ciRS-7 remarkably suppressed the proliferation, migration and invasion (all P<0.05). Conclusion: CiRS-7 was up-regulated in ESCC and could enhance ESCC cell proliferation, migration and invasion, suggesting that ciRS-7 could be used as a potential target for the diagnosis and treatment of ESCC.

Objective:To evaluate the role of mitochondria-associated endoplasmic reticulum membranes (MAMs) regulated by protein tyrosine phosphatase interacting protein 51 (PTPIP51) in sevoflurane-induced necroptosis in hippocampal neurons of rats using the in vitro experiment.Methods:Primary cultured hippocampal neurons from fetal rats of Sprague-Dawley rats were inoculated in culture wells (100 μl/well ) or culture flasks (3 ml/bottle) at a density of 5×10 5 cells/ml at 7 days of culture and divided into 4 groups ( n=19 each) using a random number table method: control group (C group), sevoflurane group (Sev group), sevoflurane+ siRNA-PTPIP51 transfection group (Sev+ siPTPIP51 group), and sevoflurane+ nonsense siRNA transfection group (Sev+ siNC group). The neurons were placed in a culture incubator containing 2% sevoflurane and incubated at 37 ℃ for 5 h in Sev, Sev+ siPTPIP51 and Sev+ siNC groups. Then neurons were collected for determination of the cell survival rate (by MTT method), cytoplasmic calcium concentration ([Ca 2+ ] i) and necroptosis rate (by flow cytometry), expression of PTPIP51, receptor-interacting protein kinase 1 (RIPK1), RIPK3, and phosphorylated mixed lineage kinase domain-like protein (p-MLKL) (by Western blot) and for microscopic examination of the partial length, endoplasmic reticulum circumference, and mitochondrial circumference of MAMs (with a transmission electron microscope). Results:Compared with group C, the activity of neurons was significantly decreased, the [Ca 2+ ] i and necroptosis rate were increased, the expression of PTPIP51, RIPK1, RIPK3 and p-MLKL was up-regulated, and the ratio of partial length of MAMs to endoplasmic reticulum perimeter and partial length of MAMs to mitochondrial perimeter were increased in group Sev ( P<0.05). Compared with group Sev, the activity of neurons was significantly increased, the [Ca 2+ ] i and necroptosis rate were decreased, the expression of PTPIP51, RIPK1, RIPK3 and p-MLKL was down-regulated, and the ratio of partial length of MAMs to endoplasmic reticulum perimeter and partial length of MAMs to mitochondrial perimeter were decreased in group Sev+ siPTPIP51 ( P<0.05), and no statistically significant changes were found in the above parameters in group Sev+ siNC ( P>0.05). Conclusions:Up-regulation of PTPIP51 expression mediates structural changes in MAMs and is involved in the process of sevoflurane-induced necroptosis in hippocampal neurons of rats.