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.

Background: miR-196b-5p expression is deregulated in many malignant tumors. Although miR-196b-5p has been implicated in the malignant transformation of colorectal cancer, its role in this specific type of cancer has not been fully explored. Thus, the present study was aimed to examine the cellular function of miR-196b-5p and its role in malignant biological behavior in colorectal cancer. Methods: miR-196b-5p expression was measured in colorectal cancer tissues and cell lines using quantitative real-time PCR. Cell counting kit-8 (CCK-8) assay and Transwell assay were used to detect proliferation, migration, and invasion in cell lines, whereas flow cytometry was applied to study apoptosis. Western blot analysis was performed to measure the protein levels. Dual luciferase reporter assay was used to investigate the interaction between miR-196b-5p and ING5. Tumor formation was evaluated in mice. Results: MiR-196b-5p was abundantly expressed in colorectal cancer tissues and cell lines, whereas ING5 was expressed at low levels. MiR-196b-5p was successfully overexpressed or knocked down in colorectal cancer cells. We found that miR-196b-5p overexpression significantly accelerated the proliferation, cell cycle, migration and invasion, while inhibited cell apoptosis in colorectal cancer cells. However, miR-196b-5p inhibitor showed the opposite effects. Moreover, ING5 overexpression or knockdown was successfully performed in colorectal cancer cells. ING5 overexpression suppressed proliferation, migration, invasion, the phosphorylation of PI3K, Akt as well as MEK, and promoted cell apoptosis, which could be reversed by ING5 knockdown. Additionally, ING5 was identified as a target of miR-196b-5p through bioinformatics analysis and a luciferase activity assay. Furthermore, ING5 knockdown could attenuate the decrease in proliferation, migration, invasion, and the protein levels of p-PI3K, p-Akt, and p-MEK, which were induced by miRNA-196b-5p inhibitor. Besides, miR-196b-5p knockdown inhibited tumor growth, whereas ING5 knockdown elevated it in vivo. Conclusions: In conclusion, miR-196b-5p promotes cell proliferation, migration, invasion, and inhibits apoptosis in colorectal cancer by targeting ING5.

Introduction Vessel wall magnetic resonance imaging can improve the evaluation of intracranial atherosclerotic disease. However, pathological validation is needed to improve vessel wall magnetic resonance imaging techniques. Human pathology samples are not practical for such analysis, so an animal model is therefore needed. Materials and methods Watanabe heritable hyperlipidemic rabbits and apolipoprotein E knockout rabbits were evaluated against New Zealand white wild-type rabbits. Evaluation of intracranial arteries was performed with vessel wall magnetic resonance imaging and pathological analysis, rating the presence and severity of disease in each segment. Two-tailed t-tests were performed to compare disease occurrence and severity prevalence among rabbit subtypes. Sensitivity and specificity were calculated to assess the diagnostic accuracy of vessel wall magnetic resonance imaging. Results Seventeen rabbits (five Watanabe heritable hyperlipidemic, four apolipoprotein E knockout and eight New Zealand white) were analysed for a total of 51 artery segments. Eleven segments (five Watanabe heritable hyperlipidemic and six apolipoprotein E knockout) demonstrated intracranial atherosclerotic disease on pathology. Disease model animals had lesions more frequently than New Zealand white animals ( P<0.001). The sensitivity and specificity of vessel wall magnetic resonance imaging for the detection of intracranial atherosclerotic disease were 68.8% and 95.2%, respectively. When excluding mild cases to assess vessel wall magnetic resonance imaging accuracy for detecting moderate to severe intracranial atherosclerotic disease lesions, sensitivity improved to 100% with unchanged specificity. Conclusion Intracranial atherosclerotic disease can be reliably produced and detected using 3T vessel wall magnetic resonance imaging-compatible Watanabe heritable hyperlipidemic and ApoE rabbit models. Further analysis is needed to characterize better the development and progression of the disease to correlate tissue-validated animal findings with those in human vessel wall magnetic resonance imaging studies.

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