LncNEN885 inhibits epithelial-mesenchymal transition by partially regulation of Wnt/ß-catenin signalling in gastroenteropancreatic neuroendocrine neoplasms.

It has been shown that long noncoding RNAs (lncRNAs) are involved in the carcinogenesis of multiple cancers. However, the roles of lncRNAs in gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) remain elusive. In the present study, we found that lncNEN885 was markedly decreased in human gastric NEN samples compared to adjacent normal tissues by transcriptome sequencing. Functionally, silencing or overexpression of lncNEN885 could not obviously affect cell proliferation or apoptosis in BON-1 or LCC-18 cells but could affect cell migration and invasion as well as wound-healing rates. Furthermore, dysregulation of lncNEN885 affected these biological functions by activating epithelial-mesenchymal transition through increased expression of Snail, vimentin, and N-cadherin as well as decreased E-cadherin levels in BON-1 and LCC-18 cells. Silencing of lncNEN885 could dramatically increase the phosphorylation of glycogen synthase kinase-3ß and decrease the expression of adenomatous polyposis coli and Axin, with the subsequent accumulation of ß-catenin. Taken together, dysregulation of lncNEN885 can regulate cell migration and invasion by activating epithelial-mesenchymal transition process partially through canonical Wnt/ß-catenin signaling in GEP-NEN cells, which may be a novel biomarker for the metastasis of GEP-NENs.

Hemorrhage and intestinal obstruction secondary to a Meckel's diverticulum: a case report.

We present one case of a 17-year-old male with ten-year history of anemia complaining of recurrent bloody stools, abdominal pain and fatigue for 3 months.The gastroscopy, colonoscopy, the-first-time double-balloon enteroscopy (DBE) through the anus and capsule endoscopy were performed with negative results. 99mTc-pertechnetate scan showed a round-like high radioactive concentration at the ileocecum. Double-balloon enteroscopy through the anus was performed again by a more-experienced endoscopic physician, the diverticulum was found at a distance of 50 cm to the ileocecal valve. Then a laparotomy was performed.

Self-assembly of rod-shaped particles in diblock-copolymer templates.

We investigate the self-assembly of hard rod-shaped particles with an affinity for A block in diblock AB copolymer templates. The results are consistent with a series of recent experimental findings. Furthermore, we construct the phase diagrams of the mixture with different aspect ratios of particles by changing the particle concentration phip and the volume fraction f of the A block. The variation of the aspect ratio in different particle concentrations will significantly influence the effective volume of the A component and consequent phase behavior of nanoparticle/copolymer hybrid systems, which may account for the emergence of some unexpected phenomena of morphological transitions. The present study provides insightful guidance to control the nanometer-length-scale structures of shaped particles for potential applications as functional devices.

Predictive value of thymidylate synthase expression in advanced colorectal cancer patients receiving fluoropyrimidine-based chemotherapy: evidence from 24 studies.

The published data about thymidylate synthase (TS) expression and its predictive value in advanced colorectal cancer (CRC) patients receiving fluoropyrimidine-based chemotherapy seemed inconclusive. To derive a more precise estimation of the relationship, a metaanalysis was performed. Studies have been identified by searching PubMed and Embase. Inclusion criteria were advanced CRC patients, received fluoropyrimidine-based chemotherapy and evaluation of TS expression and overall response rate (ORR). The relative ratio (RR) for ORR in patients with low-TS expression over those with high-TS expression with 95% confidence interval (CI) was calculated for each study as an estimation of the predictive effect of TS. A total of 24 studies including 1,112 patients were involved in this metaanalysis. The overall RR was 2.20 (95% CI, 1.82-2.66; p = 0.000). For studies evaluating TS expression in metastatic lesions, the pooled RR was 3.23 (95% CI, 2.27-4.59; p = 0.000); for studies testing TS expression in primary lesions, a pooled RR of 1.89 (95% CI, 1.45-2.48; p = 0.000) was estimated. Focusing the analysis on immunohistochemistry (IHC)-based or RTPCR-based assessments, the pooled RR was 1.83 (95% CI, 1.44-2.34; p = 0.000) and 2.96 (95% CI, 2.07-4.22; p = 0.000), respectively. The results indicated that low-TS expression tumors in advanced CRC patients were more sensitive to fluoropyrimidine-based chemotherapy. Subgroup analyses indicated that the predictive value of TS expression evaluated in metastases was more prominent than that of primary lesions, and that TS expression tested by RTPCR was also of greater predictive value than by IHC.

SGK1 inhibits cellular apoptosis and promotes proliferation via the MEK/ERK/p53 pathway in colitis.

AIM: To investigate the role of serum-and-glucocorticoid-inducible-kinase-1 (SGK1) in colitis and its potential pathological mechanisms. METHODS: SGK1 expression in mucosal biopsies from patients with active Crohn's disease (CD) and normal controls was detected by immunohistochemistry. We established an acute colitis model in mice induced by 2,4,6-trinitrobenzene sulfonicacid, and demonstrated the presence of colitis using the disease activity index, the histologic activity index and hematoxylin and eosin staining. The cellular events and potential mechanisms were implemented with small interference RNA and an inhibitor of signaling molecule (i.e., U0126) in intestinal epithelial cells (IECs). The interaction between SGK1 and the signaling molecule was assessed by co-immunoprecipitation. RESULTS: SGK1 expression was significantly increased in the inflamed epithelia of patients with active CD and TNBS-induced colitis model (0.58 ± 0.055 vs 0.85 ± 0.06, P < 0.01). At the cellular level, silencing of SGK1 by small interference RNA (siSGK1) significantly inhibited the phosphorylation of mitogen-activated protein kinase kinase 1 (MEK1) and the downstream molecule extracellular signal regulated protein kinase (ERK) 1/2, which induced the upregulation of p53 and Bcl-2-associated X protein, mediating the subsequent cellular apoptosis and proliferation in IECs. Cells treated with MEK1 inhibitor (i.e., U0126) before siSGK1 transfection showed a reversal of the siSGK1-induced cellular apoptosis. CONCLUSION: Our data suggested that SGK1 may protect IECs in colitis from tumor necrosis factor-α-induced apoptosis partly by triggering MEK/ERK activation.