Submucosal tunneling endoscopic resection: An effective and safe therapy for upper gastrointestinal submucosal tumors originating from the muscularis propria layer.

AIM: To evaluate the effectiveness and safety of submucosal tunneling endoscopic resection (STER) and compare its outcomes in esophageal and cardial submucosal tumors (SMTs) of the muscularis propria (MP) layer. METHODS: From May 2012 to November 2017, 173 consecutive patients with upper gastrointestinal (GI) SMTs of the MP layer underwent STER. Overall, 165 patients were included, and 8 were excluded. The baseline characteristics of the patients and SMTs were recorded. The en bloc resection rate, complete resection rate, residual rate, and recurrence rate were calculated to evaluate the effectiveness of STER, and the complication rate was recorded to evaluate its safety. Effectiveness and safety outcomes were compared between esophageal and cardial SMTs. RESULTS: One hundred and twelve men and 53 women with a mean age of 46.9 ± 10.8 years were included. The mean tumor size was 22.6 ± 13.6 mm. Eleven SMTs were located in the upper esophagus (6.7%), 49 in the middle esophagus (29.7%), 46 in the lower esophagus (27.9%), and 59 in the cardia (35.7%). Irregular lesions accounted for 48.5% of all lesions. STER achieved an en bloc resection rate of 78.7% (128/165) for GI SMTs with an overall complication rate of 21.2% (35/165). All complications resolved without intervention or were treated conservatively without the need for surgery. The en bloc resection rates of esophageal and cardial SMTs were 81.1% (86/106) and 72.1% (42/59), respectively (P = 0.142), and the complication rates were 19.8% (21/106) and 23.7% (14/59), respectively, (P = 0.555). The most common complications for esophageal SMTs were gas-related complications and fever, while mucosal injury was the most common for cardial SMTs. CONCLUSION: STER is an effective and safe therapy for GI SMTs of the MP layer. Its effectiveness and safety are comparable between SMTs of the esophagus and cardia.

Upregulation of microRNA-31 targeting integrin α5 suppresses tumor cell invasion and metastasis by indirectly regulating PI3K/AKT pathway in human gastric cancer SGC7901 cells.

To verify the hypothesis that upregulation of microRNA-31 (miR-31) targeting integrin α5 (ITGA5) suppresses tumor cell invasion and metastasis by indirectly regulating phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in human SGC7901 gastric cancer (GC) cells. The miRTarBase was used to predict whether ITGA5 is the target gene of miR-31, which was further confirmed by luciferase reporter gene assay. The SGC7901 GC cells were divided into five groups including the blank, miR-31 mimic, miR-31 mimic control, miR-31 inhibitor, and miR-31 inhibitor control groups. Reverse transcriptase-polymerase chain reaction (RT-PCR), western blotting, cell scratch test, and transwell assays were respectively performed in our study. TGA5 was found as the target gene of miR-31. The RT-PCR detection revealed that, compared with the blank group, ITGA5 messenger RNA (mRNA) expression decreased in the miR-31 mimic group, but increased in the miR-31 inhibitor group. The western blotting examination suggested that the expressions of ITGA5, PI3K, and AKT proteins reduced in the miR-31 mimic group, but enhanced in the miR-31 inhibitor group when compared to the blank group, respectively. The cell scratch and transwell assays indicated that the miR-31 expressions were negatively associated with GC cell migration and invasion. Besides, RT-PCR combined with western blotting demonstrated that the miR-31 expressions were higher in the normal tissues than those in the GC tissues, while the ITGA5 mRNA and protein showed lower expression in the normal tissues than they did in the GC tissues. Our study concluded that upregulation of miR-31 targeting ITGA5 may suppress tumor cell invasion and metastasis by indirectly regulating PI3K/AKT signaling pathway in human SGC7901 GC cells.

[Effect of silencing AEG-1 with small interfering RNA on the proliferation and cell cycle of gastric carcinoma SGC-7901 cells].

OBJECTIVE: To explore the effect of down-regulation of astrocyte elevated gene-1 (AEG-1) expression on cell proliferation and cell cycle of gastric carcinoma cells, and its possible molecular mechanism. METHODS: Control siRNA and AEG-1 siRNA were transfected into gastric carcinoma SGC-7901 cells. 48 h after transfection, the cells were divided into 3 groups including untransfected, siRNA control and AEG-1 siRNA transfection groups. Expressions of AEG-1 mRNA and protein in the 3 group cells were detected by real-time quantitative PCR and Western blot. The changes of cell proliferation were examined using CCK-8 kit, and the cell cycle distribution was detected by flow cytometry. Finally, expressions of cell proliferation and cell cycle related proteins were detected by Western blot. RESULTS: Real-time quantitative PCR and Western blot demonstrated that compared with the untransfected and siRNA control groups, expressions of AEG-1 mRNA and protein were significantly down-regulated in the AEG-1 siRNA transfection group (P < 0.05), but there was no significant difference between the untransfected and siRNA control groups (P > 0.05). Furthermore, in vivo experiment confirmed a significant down-regulation of AEG-1 protein in the AEG-1 siRNA transfection group (P < 0.05). In addition, AEG-1 siRNA obviously inhibited the proliferation of SGC-7901 cells at different time points after transfection with AEG-1 siRNA. The percentage of cells in G0/G1 phase in the AEG-1 siRNA transfection group [(61.26 ± 1.25)%] was significantly higher than those in the untransfected group [(46.17 ± 1.91)%] and siRNA control group [(46.46 ± 1.96)%], and there was a significant difference between them (all P < 0.001). Furthermore, the result of Western blotting revealed that down-regulation of AEG-1 expression evoked the down-regulation of cdk2 and cyclin D1 expressions and elevation of p21 expression in vitro and in vivo. CONCLUSIONS: The inhibition of cell proliferation and cell cycle arrest mediated by down-regulation of AEG-1 expression may be closely associated with the changes of expression of cell cycle related proteins including cdk2, cyclin D1 and p21.

[Efficacy of probiotics on ulcerative colitis and its mechanism].

OBJECTIVE: To evaluate the efficacy of probiotics on the treatment outcomes of ulcerative colitis, and explore its possible mechanism. METHODS: According to the table of random number, 60 ulcerative colitis patients in our hospital were enrolled prospectively and divided into 3 groups: Golden Bifid group, Changmei group, combination group (Golden+ Changmei). Patients in Golden Bifid group received Golden Bifid 2.0 g, bid, those in Changmei group received Changmei 1.0 g, tid, and those in combination group received the above two drugs for 24 months. The clinical symptom score, colon mucosa inflammation score and endoscopic grade score were calculated and compared. IL-10 in mucosa and serum was determined by immunohistochemistry and double-antibody sandwich ELISA. RESULTS: In combined group after 24 months of treatment, clinical symptom score (12.5±2.1 vs. 2.3±0.8, P=0.016), endoscopic classification score (3.02±0.17 vs. 0.25±0.13, P=0.032), inflammatory reaction score (2.63±0.19 vs. 0.77±0.16, P=0.028) were significantly higher than those before treatment. While the scores differences of before and after treatment in Gold Bifid group and Changmei group were not statistically significant (P>0.05). IL-10 in serum [(17.4±2.2) ng/L vs. (12.8±2.2) ng/L, P=0.015] and colon mucosa [85% (17/20) vs. 55% (11/20), P=0.026] in combination group were significantly higher than those before treatment. The differences in IL-10 expression level before and after treatment were not statistically significant in the Gold Bifid group and Changmei group (P>0.05). CONCLUSION: Golden Bifid combined with Changmei as microbial ecological agents has a positive efficacy on mild to moderate ulcerative colitis, which may be associated with the up-regulation of IL-10 expression.

[Effects of KIAA0101 expression on proliferation and invasion of gastric carcinoma MKN-45 cells].

OBJECTIVE: To investigate the expression of KIAA0101 protein in gastric carcinoma cells, and to explore the effects of its down-regulation on the cell proliferation, cell cycle and invasion. METHODS: Western blot was used to detect KIAA0101 protein expression in three gastric carcinoma cell lines including MKN-28, SGC-7901 and MKN-45. KIAA0101 siRNA and control siRNA were utilized to transfect MKN-45 cells, respectively. CCK-8 was used to analyze the changes of cell proliferation, and flow cytometry to examine the changes of cell cycle distribution. Finally, Boyden chamber was used to detect the ability of cell invasion. RESULTS: Relative level of KIAA0101 protein in MKN-45 cells was significantly higher than those in MKN-28 and SGC-7901 cells, and there was significant difference among the three cell lines (P < 0.05). The result of CCK-8 study demonstrated that, compared with untreated group and control siRNA group, the proliferation of MKN-45 cells in KIAA0101 siRNA group was significantly inhibited (P < 0.05). Additionally, the result of cell cycle analysis revealed that the percentage of cell number in G(0)/G(1) phase in KIAA0101 siRNA group [(61.47 ± 0.89)%] was significantly higher than those in untreated group [(47.43 ± 0.85)%] and control siRNA group [(48.43 ± 0.73)%; F = 271.653, P = 0.000]. Further, Boyden chamber assay showed that the cell numbers migrated to Matrigel in KIAA0101 siRNA group (61.51 ± 4.76) were significantly lower than those in untreated group (138.74 ± 10.16) and control siRNA group (132.93 ± 11.25; F = 65.949, P = 0.000). CONCLUSIONS: Down-regulation of KIAA0101 expression leads to an inhibition of cell proliferation, cell cycle and cell invasion. It may provide a novel target for the treatment of patients with gastric carcinoma.