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.

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BACKGROUND Surgical resection is considered the standard treatment option for long-term survival in colorectal cancer liver metastasis (CRLM) patients, but only a small number of patients are suitable for resection following diagnosis. Radiofrequency ablation (RFA) is an accepted alternative therapy for CRLM patients who are not suitable for resection. However, the relatively high rate of local tumor progression (LTP) is an obstacle to the more widespread use of RFA. AIM To determine the oncological outcomes and predictors of RFA in CRLM patients. METHODS A retrospective analyze was performed on the clinical data of 85 consecutive CRLM patients with a combined total of 138 liver metastases, who had received percutaneous RFA treatment at our institution from January 2013 to December 2018. Contrast-enhanced computed tomography was performed the first month after RFA to assess the technique effectiveness of the RFA and to serve as a baseline for subsequent evaluations. The Kaplan-Meier method was used to calculate overall survival (OS) and LTP-free survival (LTPFS). The log-rank test and Cox regression model were used for univariate and multivariate analyses to determine the predictors of the oncological outcomes. RESULTS There were no RFA procedure-related deaths, and the technique effectiveness of the treatment was 89.1% (123/138). The median follow-up time was 30 mo. The LTP rate was 32.6% (45/138), and the median OS was 36 mo. The 1-, 3-, and 5-year OS rates were 90.6%, 45.6%, and 22.9%, respectively. Univariate analysis revealed that tumor size and ablative margin were the factors influencing LTPFS, while extrahepatic disease (EHD), tumor number, and tumor size were the factors influencing OS. Multivariate analysis showed that tumor size larger than 3 cm and ablative margin of 5 mm or smaller were the independent predictors of shorter LTPFS, while tumor number greater than 1, size larger than 3 cm, and presence of EHD were the independent predictors of shorter OS. CONCLUSION RFA is a safe and effective treatment method for CRLM. Tumor size and ablative margin are the important factors affecting LTPFS. Tumor number, tumor size, and EHD are also critical factors for OS.

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Breast cancer (BC) is the most commonly diagnosed malignant cancer in women. BC is the main cause of cancer-related death in women and seriously threatens the life and health of women worldwide. MicroRNAs (miRNAs/miRs) have been reported to regulate the development and progression of different types of cancer. However, the regulatory functions of miR-188-5p in BC have not been thoroughly demonstrated. In this present research, we identified that miR-188-5p was downregulated in BC tissues and several BC cell lines. Downregulation of miR-188-5p was significantly associated with advanced TNM stage. Moreover, we identified that miR-188-5p mimics significantly inhibited proliferation using CCK-8 assay, colony formation and xenograft animal model, suppressed invasion and migration detected by Transwell invasion assay, and increased the cellular apoptosis of BC cells as determined by cell apoptosis assay. Moreover miR-188-5p mimics also reduced the expression of NF-κB p65(Rel). To further investigate its regulatory mechanism, transcription factor zinc finger protein 91 (ZFP91) was predicted as the targeted protein of miR-188-5p by bioinformatic method. We confirmed their specific binding by dual luciferase (DLR) assay. We demonstrated that the overexpression of miR-188-5p significantly inhibited the expression of ZFP91 in BC cell lines and reduced the expression of NF-κB p65(Rel). An inverse correlation was found between the expression of miR-188-5p and ZFP91 in BC tissues. Importantly, we demonstrated that the restoration of ZFP91 was able to block the effect of miR-188-5p on the progression of MDA-MB-231 cells. Therefore, our study showed that miR-188-5p may be one of the important indicators and could inhibit the progression of human BC via targeting the ZFP91/NF-κB p65(Rel) signaling pathway, suggesting that miR-188-5p may be a promising future target for BC treatment.