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Propofol is a commonly used drug for the induction and maintenance of anesthesia. Previous studies have reported that propofol is involved in the progression of numerous human cancer types, including hepatocellular carcinoma (HCC). However, the underlying molecular mechanisms in HCC are yet to be elucidated. The present study aimed to investigate the potential mechanism of propofol in HCC development. MTT assay, flow cytometry analysis and Transwell assays were conducted to examine cell proliferation, apoptosis, migration and invasion, respectively. Western blotting was also performed to determine the protein expression levels of Bcl-2 and cleaved-caspase 3. An in vivo experiment was performed to assess the effect of propofol on tumor growth. Moreover, reverse transcription-quantitative PCR was conducted to measure the mRNA expression levels of HOMEOBOX A11 (HOXA11) antisense RNA (HOXA11-AS) and microRNA (miR)-4458. Dual-luciferase reporter and RNA pull-down assays were performed to evaluate the target relationship between HOXA11-AS and miR-4458. It was demonstrated that propofol inhibited HCC cell proliferation, migration and invasion, and promoted cell apoptosis in vitro. Furthermore, propofol could suppress tumor growth in vivo. Propofol suppressed the expression of HOXA11-AS in HCC cells, while HOXA11-AS overexpression reversed the inhibitory effect of propofol treatment on cell progression in HCC. In addition, miR-4458 was identified as a target of HOXA11-AS, and miR-4458 inhibition reversed the effect of HOXA11-AS knockdown on HCC cell progression. The results also indicated that propofol promoted the expression of miR-4458, while HOXA11-AS restored this effect in HCC. Thus, it was suggested that propofol suppressed cell progression by modulating the HOXA11-AS/miR-4458 axis in HCC.

In-stent restenosis (ISR) can pose serious challenges for cardiologists following coronary stent implantation. Early identification of patients at high risk of ISR is considered to be effective for its prevention. However, factors that can reliably predict the risk of ISR remain elusive at present. The present study aimed to investigate the possible association between plasma long non-coding RNA (lncRNA) levels and ISR. A total of 410 patients with single-vessel lesion who received drug-eluting stents (DES) were included in the present study. After 12-36 months of follow-up, coronary angiography was performed and ISR was defined as >50% diameter stenosis at follow-up. RT-qPCR was used to measure lncRNA expression. Expression of the lncRNA RNA antisense non-coding RNA at the INK4 locus (ANRIL) was found to be upregulated whereas the lncRNA homeobox A11 antisense (HOXA11-AS) was downregulated in the plasma of patients with ISR compared with that from patients without ISR (P<0.001). Logistic regression analysis revealed that ANRIL [odds ratio (OR)=2.95; 95% confidence interval (CI)=1.68-8.08] was an independent risk factor for ISR, whilst HOXA11-AS (OR=0.58; 95% CI=0.48-0.71) was found to be an independent protective factor for ISR. Receiver operating characteristic (ROC) analysis demonstrated that high ANRIL expression [area under the ROC (auROC)=0.755; 95% CI=0.702-0.803] and low HOXA11-AS levels (auROC=0.712; 95% CI=0.657-0.763) predicted a high risk for ISR, and the combined score of ANRIL and HOXA11-AS (auROC=0.844; 95% CI=0.798-0.884) was more efficient at predicting ISR than either ANRIL or HOXA11-AS alone (P<0.001). In conclusion, increased ANRIL and decreased HOXA11-AS expressions were associated with ISR. However, combined ANRIL and HOXA11-AS plasma levels proved to be more effective at predicting ISR compared with either ANRIL or HOXA11-AS alone, suggesting that the multiplex detection of lncRNAs could be used to predict ISR in the future.

Cardiac fibrosis is closely associated with various heart diseases and is an important pathological feature of cardiac remodeling. However, detailed mechanisms underlying cardiac fibrosis remain largely unknown. Long noncoding RNAs (lncRNAs) are reported to serve significant roles in the development of cardiac fibrosis. The present study aimed to identify the role of a novel lncRNA, homeobox A11 antisense (HOXA11-AS), in cardiac fibrosis. Overexpression of HOXA11-AS in mouse cardiac fibroblasts (CFs) increased the expression of transforming growth factor β1 (TGFβ1) and its downstream molecules, while knockdown of HOXA11-AS inhibited the TGFβ1 signaling pathway. Furthermore, as determined by colony formation and MTT assays, HOXA11-AS overexpression promoted colony formation and viability in mouse CFs, while HOXA11-AS knockdown had the opposite effect. In addition, overexpression of HOXA11-AS increased cell migration and invasion in the Transwell assays, whereas expression knockdown decreased the metastatic ability of cells. In order to explore the detailed mechanism, co-transfection of HOXA11-AS expression plasmid and siTGFβ1 into CFs resulted in increased cell proliferative rate and cell metastasis through the TGFβ1 signaling pathway. Taken together, the present study suggested that the lncRNA HOXA11-AS may be a potential therapeutic target against cardiac fibrosis, and provided a novel insight into the diagnosis and treatment of clinical cardiac fibrosis.