Small Extracellular Vesicle piR-hsa-30937 Derived from Pancreatic Neuroendocrine Neoplasms Upregulates CD276 in Macrophages to Promote Immune Evasion.

The role of PIWI-interacting RNAs (piRNA) in small extracellular vesicles (sEV) derived from pancreatic neuroendocrine neoplasms (PNEN) in the tumor microenvironment (TME) remains unexplored. We used multiplex IHC to analyze the expression of CD68, CD276 (B7H3), and CD3 on PNEN. CD276+ tumor-associated macrophages (TAM) were more abundant in tumor tissues than nontumor tissues and negatively correlated with T-cell infiltration.

Prognostic Evaluation of Patients with Rectal Neuroendocrine Neoplasms and Hepatic Metastases: A SEER Database Analysis.

Background: This study is aimed at investigating the clinical characteristics and prognosis-affecting factors of patients with rectal neuroendocrine neoplasms (r-NENs) and hepatic metastases and offering a scientific-theoretical basis for selective use of an optimized treatment method for r-NENs.

Methods: This study was retrospectively evaluated based on the analysis of the data from Surveillance, Epidemiology, and End Results (SEER) database between 2010 and 2016.

Results: A total of 4,723 r-NEN patients were enrolled in this study, including 168 patients with hepatic metastases (3.

Trends of incidence and prognosis of gastric neuroendocrine neoplasms: a study based on SEER and our multicenter research.

Background: To investigate the recent epidemiological trends of gastric neuroendocrine neoplasms (GNENs) and establish a new tool to estimate the prognosis of gastric neuroendocrine carcinoma (GNEC) and gastric neuroendocrine tumor (GNET).

Methods: Nomograms were established based on a retrospective study on patients diagnosed with GNENs from 1975 to 2016 in Surveillance, Epidemiology and End Results database. External validation was performed among 246 GNENs patients in Jiangsu province to verify the discrimination and calibration of the nomograms.

LncNEN885 inhibits epithelial-mesenchymal transition by partially regulation of Wnt/β-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.

Anticancer Effects of Baicalein in Pancreatic Neuroendocrine Tumors In Vitro and In Vivo.

Objectives: Baicalein is a Chinese traditional medicine that inhibits tumor migration and growth. Pancreatic neuroendocrine tumors (pNETs) have a high incidence in China, but there are still no effective treatments. The aim of our study was to investigate whether baicalein could inhibit pNETs.

Chromosome region maintenance-1 (CRM1) regulates apoptosis of intestinal epithelial cells via p27kip1 in Crohn's disease.

Objective: To investigate the role of chromosome region maintenance-1 (CRM1) in Crohn's disease (CD) and its potential pathological mechanisms.

Methods: The expression and distribution of CRM1 in mucosal biopsies from patients with active CD and normal controls were detected by immunohistochemistry (IHC). We established a murine model of acute colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS).

Microtubule-associated protein 1S-related autophagy inhibits apoptosis of intestinal epithelial cells via Wnt/β-catenin signaling in Crohn's disease.

Many autophagy-related genes, to our knowledge, have been identified as Crohn's disease (CD) polymorphic sites by genomic wide studies. As a novel member of the microtubule-associated protein 1 (MAP1) family, MAP1S is a microtubule-binding proteins involved in autophagy. However, its expression and potential functions in CD have not been understood.

A retrospective study of NENs and miR-224 promotes apoptosis of BON-1 cells by targeting PCSK9 inhibition.

Neuroendocrine neoplasms (NENs) represent relatively rare tumors. The lack of diagnostic, therapeutic method and prognostic factors makes them a challenge to us. We retrospectively reviewed the data of 205 NENs patients among which 157 cases were followed-up.

GART mediates the renewal of intestinal epithelial barrier via p38/p53/PUMA cascade in colitis.

Glycinamide ribonucleotide formyltransferase (GART) has been established as a pivotal enzyme in de novo purine synthesis, and mediates cellular apoptosis in many diseases. We aimed to investigate the role of GART in the pathogenesis of Crohn's disease (CD). In our study, we demonstrated for the first time that GART expression is up-regulated in patients with active CD and in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced acute colitis model.

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.

Role of far upstream element binding protein 1 in colonic epithelial disruption during dextran sulphate sodium-induced murine colitis.

Aim: Intestinal epithelial barrier is essential for maintaining normal intestinal homeostasis; its breakdown leads to chronic inflammatory pathologies, such as inflammatory bowel diseases. Far upstream element binding protein 1 (FBP1) has been reported to play an important role in cell apoptosis and proliferation. We aimed to investigate the expression and the role of FBP1 in dextran sodium sulphate (DSS)-induced experimental colitis.

Pyruvate kinase M2 regulates apoptosis of intestinal epithelial cells in Crohn's disease.

Background: Pyruvate kinase M2 (PKM2), a key glycolytic enzyme, is involved in multiple cellular processes including apoptosis. Recently increased fecal PKM2 has been found in Crohn's disease (CD), but little is known regarding its function in the pathophysiology of the disease.

Aim: The intestinal expression of PKM2 and its involvement in CD was investigated.