BackgroundMicroRNA-196a-5p (miR-196a-5p) has been reported to be involved in the metastatic process of several cancers. In present work, we aimed to investigate the effects of miR-196a-5p and its potential target IκBα on migration, invasion and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells.MethodsCCK-8 assay, wound healing assay and cell invasion assay were performed to evaluate the cell proliferation, migration and invasion. In vivo metastasis models were used to investigate the tumor metastasis ability. Real-time PCR, immunofluorescence staining or western blot were utilized to detect the expression of miR-196a-5p, IκBα, p-IκBα, nuclear p65 and EMT markers including E-cadherin, N-cadherin and fibronectin. Dual luciferase reporter assay was carried out to determine whether there is a direct interaction between miR-196a-5p and IκBα mRNA.ResultsUsing SW480 cell with miR-196-5p over-expressed plus SW620 and HCT116 cells with miR-196a-5p knockdown, we found that miR-196a-5p promoted cell proliferation, migration and invasion in vitro and facilitated liver metastasis in vivo. We also observed that miR-196a-5p knockdown or NF-κB pathway inhibition up-regulated E-cadherin while down-regulated N-cadherin and fibronectin. By contrast, miR-196a-5p over-expression promoted EMT process of CRC. Data of dual luciferase reporter assay indicated that miR-196a-5p targeted the IκBα. Moreover, miR-196a-5p down-regulated IκBα expression while up-regulated nuclear p65 expression. Additionally, over-expression of IκBα in CRC cells attenuated the effects of miR-196a-5p on cell migration, invasion and EMT.ConclusionsmiR-196a-5p may play a key role in EMT, invasion and metastasis of CRC cells via targeting the IκBα.Electronic supplementary materialThe online version of this article (10.1186/s12885-018-5245-1) contains supplementary material, which is available to authorized users.

Perivascular epithelioid cell tumor (PEComa) is a rare tumor. Here, we present data regarding clinical presentations, diagnoses, management, and prognosis of five cases of hepatic PEComa between January 2002 and December 2008. Ultrasonography showed hyperechoic masses in all patients. Precontrast computed tomography (CT) showed that all lesions scanned were heterogeneous in density and were heterogeneously enhanced in arterial phase images. In two cases, magnetic resonance imaging showed hypointensity on T1-weighted images and hyperintensity on T2-weighted images. In enhanced scanning, lesions showed asymmetrical enhancement during arterial phase imaging. All tumors were composed of varying proportions of smooth muscle, adipose tissue, and thick-walled blood vessels, and showed positive immunohistochemical staining for Human Melanoma Black-45. All patients underwent hepatectomy, and there was no evidence of recurrence or metastasis during the follow-up period.

BACKGROUNDLong non-coding RNAs (lncRNAs) play important roles in many diseases, including hepatocellular carcinoma (HCC). Autophagy is a metabolic pathway that facilitates cancer cell survival in response to stress. The relationship between autophagy and the lncRNA-activated by transforming growth factor beta (lncRNA-ATB) in HCC remains unknown.AIMTo explore the influence of lncRNA-ATB in regulating autophagy in HCC cells and the underlying mechanism.METHODSIn the present study, we evaluated lncRNA-ATB expression in tumor and adjacent non-tumor tissues from 72 HCC cases by real-time PCR. We evaluated the role of lncRNA-ATB in the proliferation and clonogenicity of HCC cells in vitro. The effect of lncRNA-ATB on autophagy was determined using a LC3-GFP reporter and transmission electron microscopy. Furthermore, the mechanism by which lncRNA-ATB regulates autophagy was explored by immunofluorescence staining, RNA immunoprecipitation (RIP), and Western blot.RESULTSThe expression of lncRNA-ATB was higher in HCC tissues than in normal liver tissues, and lncRNA-ATB expression was positively correlated with tumor size, TNM stage, and poorer survival of patients with HCC. Moreover, ectopic overexpression of lncRNA-ATB promoted cell proliferation and clonogenicnity of HCC cells in vitro. LncRNA-ATB promoted autophagy by activating Yes-associated protein (YAP). Moreover, lncRNA-ATB interacted with autophagy-related protein 5 (ATG5) mRNA and increased ATG5 expression.CONCLUSIONLncRNA-ATB regulates autophagy by activating YAP and increasing ATG5 expression. Our data demonstrate a novel function for lncRNA-ATB in autophagy and suggest that lncRNA-ATB plays an important role in HCC.

Intracranial atherosclerotic disease (ICAD) is the most common cause of stroke worldwide. [1][2][3] Pathophysiological mechanisms of ICAD have not been clarified in a way that is specific to intracranial disease, so current clinical management strategies are suboptimal.Better understanding of ICAD is needed through basic science and translational research to develop more effective treatment. A major hindrance in the study of ICAD pathophysiology is the lack of tissue for pathological evaluation, but this cannot be reliably obtained in humans. Biopsy is prohibitively morbid, so tissue is typically only obtained at autopsy. Given limitations in human investigation of ICAD, current management is based on extrapolation from extracranial disease. Such extrapolation may be flawed since intracranial and extracranial vessels arise from different germ cell layers, ectoderm, and mesoderm,

The purpose of this study was to assess the value of the neutrophil-to-lymphocyte ratio (NLR) as a predictive factor for recurrence of colorectal liver metastases following radiofrequency ablation (RFA) treatment. We retrospectively analyzed clinical data from 98 patients who received routine RFA treatment for colorectal liver metastases. Univariate analyses were conducted to evaluate the effects of preoperative maximum tumor diameter, number of tumors, colon cancer staging, carcinoembryonic antigen levels, and preoperative and postoperative NLRs on disease-free survival (DFS). Statistically significant factors were further analyzed using multivariate Cox regression models to identify independent factors that were predictive of tumor recurrence. The one-, three-, and five-year DFS rates for patient were 66.3, 28.6, and 17.3%, respectively. Univariate analysis showed that preoperative NLR≥2.5 and postoperative increase in NLR were associated with decreased DFS rates. One-, three-, and five-year DFS rates for patients with preoperative NLR≥2.5 were 53.3, 20.0, and 11.1%, whereas patients with preoperative NLR<2.5 had DFS rates of 77.4, 35.8, and 22.6%, respectively (P=0.044). One-, three- and five-year DFS rates for patients with NLRs increased 1 month after RFA treatment were 52.3, 17.1, and 8.6%, while patients with no increased postoperative NLRs had DFS rates of 73.0, 34.9, and 22.2%, respectively (P=0.022). Cox regression analysis showed that postoperative NLR increase was an independent risk factor (P=0.029) for recurrence after RFA treatment in patients with colorectal liver metastases. The present study suggests that patients with preoperative NLRs≥2.5 or increased postoperative NLR are at an increased risk for recurrence after RFA treatment for colorectal liver metastases.