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Intracarotid cold saline infusion (ICSI) brings about neuroprotective effects in ischemic stroke. However, the involvement of serum and glucocorticoid-regulated kinase 1 (SGK1) in the underlying mechanism of ICSI is not fully understood; therefore, we used the rat middle cerebral artery occlusion (MCAO) model to investigate the neuroprotective effects of ICSI on ischemic stroke in rats, as well as the involvement of SGK1 in these effects. ICSI decreased infarct size and brain swelling, as determined by 2,3,5-triphenyltetrazolium chloride staining and the dry-wet weight method, respectively. The results of terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) and Nissl staining showed that ICSI also suppressed apoptosis and increased the relative integral optical density (IOD) values of Nissl bodies in the rat MCAO model. Regarding the mechanism, the results of immunohistochemistry and western blotting revealed that ICSI upregulated SGK1 expression and downregulated beclin-1 and LC-3 expression in the rat MCAO model. In addition, SGK1 knockdown increased ICSI-mediated infarct size and brain swelling, promoted apoptosis, and reduced the IOD values of Nissl bodies in the rat MCAO model. In addition, we found that SGK1 knockdown upregulated beclin-1 and LC-3 expression mediated by ICSI. Overall, ICSI had a neuroprotective effect on ischemic stroke after reperfusion by upregulating SGK1 and inhibiting autophagy. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is the third leading cause of cancer‑associated mortality in the 21st century. microRNA (miR)‑23b has been shown to be involved in the pathogenesis of many cancers, including breast and prostate cancer. However, the role of miR‑23b in HCC remains unclear. The present study revealed a negative correlation between miR‑23b expression in HCC tissues and progression of carcinomas. Compared to normal tissues, miR‑23b expression was significantly downregulated in HCC tissues, whereas the expression of interleukin (IL)‑11 and IL‑11 receptor α (IL‑11Rα) was significantly upregulated, indicating that miR‑23b expression is negatively correlated with IL‑11 and IL‑11Rα expression. In addition, miR‑23b inhibited proliferation and promoted apoptosis of SMMC‑7721 cells. This effect was mediated by IL‑11, which was found to be the direct target of miR‑23b in this study. These results indicated that miR‑23b regulates IL‑11 and IL‑11Rα expression, and might act as an anti‑oncogenic agent in the progression of HCC by directly downregulating IL‑11 expression. [ABSTRACT FROM AUTHOR]

The present study aimed to assess the B rapidly accelerated fibrosarcoma (BRAFV600E) status in plasma from Chinese patients with melanoma, and evaluated its prognostic value following treatment with BRAF inhibitors. Mutation-specific 3D digital polymerase chain reaction (dPCR) was used to quantify BRAFV600E in circulating tumor DNA (ctDNA) in 58 patients with melanoma, prior to treatment with BRAF inhibitors. Correlations between baseline ctDNA levels and clinicopathological characteristics and clinical benefits were then statistically analyzed. The concordance and sensitivity of BRAFV600E between ctDNA and tumor tissue were 70.2% and 76%, respectively, in 58 patients with melanoma. BRAFV600E mutation in ctDNA correlated with lactate dehydrogenase concentration (P=0.04) and Eastern Cooperative Oncology Group score (P=0.04). There was no correlation between BRAFV600E of ctDNA with response, progression-free survival (PFS), or overall survival (OS) following targeted therapy. The objective response rate, PFS and OS stratified by BRAFV600E of ctDNA were 30.0% vs. 56.7%, (P=0.3), 8.1 months vs. 6.7 months, (P=0.38) and 65.6 months vs. 42.3 months (P=0.52), respectively, for undetectable and mutant types. In conclusion, 3D dPCR is appropriate for ctDNA detection and BRAFV600E in ctDNA is a non-invasive biomarker in patients with melanoma. [ABSTRACT FROM AUTHOR]