LINC00665 up-regulates SIN3A expression to modulate the progression of colorectal cancer via sponging miR-138-5p.

BACKGROUND: Colorectal cancer (CRC) is a malignant tumor affecting people worldwide. Long noncoding RNAs (lncRNAs) is a crucial factor modulating various cancer progression, including CRC. Long intergenic non-protein coding RNA 665 (LINC00665) has been proven as an oncogene in several cancers, but its function in CRC is still unclear. METHODS: QRT-PCR was performed for RNA quantification. Functional assays were designed and carried to test cell phenotype while mechanism experiments were adopted for detecting the interaction of LINC00665, microRNA-138-5p (miR-138-5p) and SIN3 transcription regulator family member A (SIN3A). In vivo experiments were conducted to test LINC00665 function on modulating CRC tumor progression. RESULTS: LINC00665 displayed high expression in CRC tissues and cells, and promoted tumor progression in vivo. MiR-138-5p displayed abnormally low expression in CRC, and was verified to be sponged by LINC00665. Furthermore, SIN3A, as the downstream mRNA of miR-138-5p, exerted promoting impacts on CRC cells. Rescue experiments certified that overexpressed SIN3A or silenced miR-138-5p could offset the repressed function of LINC00665 knockdown on CRC progression. CONCLUSIONS: LINC00665 could sponge miR-138-5p to up-regulate SIN3A expression, thus accelerating CRC progression.

Long Intergenic Non-Protein-Coding RNA 01138 Accelerates Tumor Growth and Invasion in Gastric Cancer by Regulating miR-1273e.

BACKGROUND The treatment and nursing of gastric cancer (GC) remains an enormous challenge in clinical practice. Understanding the potential mechanisms of the pathogenesis of GC would improve GC therapy. Long intergenic non-protein-coding RNA 01138 (LINC01138) was reported to promote the progression of hepatocellular carcinoma; however, whether it is involved in GC progression has been unclear. MATERIAL AND METHODS Expressions of LINC01138 and miR-1273e in GC tissues and cell lines were measured by qRT-PCR assay. The interaction between LINC01138 and miR-1273e was predicted by the online tool miRDB, verified by dual-luciferase reporter and RNA pulldown assays. Effects of LINC01138 knockdown or miR-1273e overexpression on cell viability, proliferation, apoptosis, invasion, and migration were evaluated by MTT, colony formation assay, flow cytometry, and Transwell assays. Target genes of miR-1273e were predicted by KEGG analysis, and involvement of the mitogen-activated protein kinase (MAPK) pathway was confirmed by qRT-PCR assay. RESULTS LINC01138 was increased but miR-1273e was decreased in GC tissues and cell lines. Knockdown of LINC01138 suppressed GC cell viability, proliferation, invasion, and migration, and promoted GC cell apoptosis. We demonstrated that LINC01138 contributed to GC progression by directly sponging and inhibiting miR-1273e. Moreover, the MAPK pathway was verified to participate in the promotive effects of LINC01138 on GC progression. CONCLUSIONS LINC01138 activated the MAPK signaling pathway by inhibiting miR-1273e to promote GC cell proliferation, invasion, and migration, and inhibit GC cell apoptosis, suggesting that the LINC01138/miR-1273e/MAPK axis is a promising therapeutic target for GC.

High frequency stimulation of the STN restored the abnormal high-voltage spindles in the cortex and the globus pallidus of 6-OHDA lesioned rats.

Many studies showed that abnormal oscillations in the cortical-basal ganglia loop is involved in the pathophysiology of Parkinson's disease (PD). In contrast to the well-studied beta synchronization, high-voltage spindles (HVSs), another type of abnormal oscillation observed in PD, are neglected. To explore the role of subthalamic nucleus-deep brain stimulation (STN-DBS) in HVSs regulation, we simultaneously recorded the local field potential (LFP) in the globus pallidus (GP) and electrocorticogram (ECoG) in the primary motor cortex(M1) in freely moving 6-hydroxydopamine (6-OHDA) lesioned or control rats before, during, and after STN-DBS. Consistent with our previous study, HVSs occurrence, duration, and relative power and coherence between the M1 cortex and GP increased in 6-OHDA lesioned rats. We found that high but not low frequency stimulation restored the abnormal HVSs activity and motor deficit. These results suggest that the STN is involved in the abnormal oscillation between the M1 cortex and GP.

[The difference in diagnosis rate of different diagnostic criteria of autoimmune pancreatitis and its major influential factors].

OBJECTIVE: To discuss the difference in diagnostic criteria of autoimmune pancreatitis(AIP) and its major influential factors, so as to provide guidance for AIP diagnosis and treatment. METHODS: The clinical data of 561 cases of chronic pancreatitis admitted to PLA General Hospital from June, 2008 to January, 2013 were retrospectively reviewed and analyzed. Data were extracted and analyzed to summarize the reasons of the differences in AIP diagnosis rate diagnosed by different diagnostic criteria. RESULTS: A total of 34 cases were eligible for the 2006 American HISORt criteria of AIP of whom, 5, 10 and 26 met the criteria of histology, pancreatic imaging findings and increasing serum IgG4 levels, and response to steroids and increasing serum IgG4 levels, respectively. Seven AIP patients met the latter two criteria. Fifteen patients were eligible for the 2008 Asian diagnostic criteria for AIP, of which, 10 met the two necessary imaging findings and 5 met the criteria of pathology of lymphoplasmacytic sclerosing pancreatitis (LPSP) after surgical resection. CONCLUSIONS: AIP is characterized by autoimmune inflammatory process, and is easy to be misdiagnosed as pancreatic cancer or cholangiocarcinoma etc. As a few sets of criteria issued from different countries, the 2008 Asian diagnostic criterion is more suitable with Chinese population. We should pay full attention to the importance of imaging examination of the diagnosis of AIP on the base of the detection of immune parameters, pathological examination and response to steroids.