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Cirrhosis and portal hypertension are associated with an increased risk of developing liver cancer. However, it is unknown how changes in the cellular mechanical microenvironment induced by portal hypertension affect the occurrence and development of liver cancer. The aim of this study was to determine the effect of tensile strain on the proliferation of a human liver cancer cell line (HepG2 cells) using methods such as flow cytometry, Cell Counting Kit-8 and 5-bromodeoxyuridine assays, and to examine the changes in microRNA (miRNA/miR) expression using microarray, reverse transcription-quantitative (RT-q)PCR and bioinformatics analyses. It was demonstrated that cyclic tensile force promoted the proliferation of HepG2 cells. The most suitable research conditions were as follows: Tensile strain force loading amplitude 15%; frequency 1 Hz; and time 24 h. After loading the HepG2 cells under such conditions, the differentially expressed miRNAs were screened out using an Agilent Human miRNA Microarray, identifying seven miRNAs with significant differences (expression difference >2 times and P

Skeletal muscle plays an important role in the growth and development of meat animals. MicroRNAs (miRNAs) can participate in the regulation of muscle development-related functions; however, there have been few reports on whether there are related miRNAs that conservatively regulate muscle development among different species. In this study, the miRNA transcriptome sequencing data of the muscle tissue of cattle, rat, goat, and pig showed that miR-24-3p may conservatively regulate muscle development in these species. Furthermore, mmu-miR-24-3p can positively regulate C2C12 cell proliferation and apoptosis by regulating key proliferation and apoptosis genes in muscle development, which was verified by CCK-8 and RT-qPCR. Bta-miR-24-3p can also positively regulate the proliferation and apoptosis of bovine muscle primary cells by regulating key proliferation and apoptosis genes in the process of muscle development, as verified by CCK-8 and RT-qPCR. The target genes of miR-24-3p in cattle, rat, goat, and pig, which include a large proportion of target genes shared among the four species, are enriched in multiple cell functions and signal pathways that are closely related to muscle development, as revealed by GO and KEGG enrichment analysis. A double luciferase test showed that the shared target genes WNT4, CAMK2B, and TCF7 were targeted by mmu-miR-24-3p in rat and bta-miR-24-3p in cattle. These three shared target genes WNT4, CAMK2B, and TCF7 are involved in the Wnt signaling pathway, which showed that miR-24-3p plays an important role in rat and cattle. The shared target gene (CAMK2B) in rat and cattle increased significantly after the inhibition of miR-24-3p by RT-qPCR. The findings of this study contribute to a better understanding of the role of miR-24-3p in the regulation of muscle development.

// Hua Guo 1, * , Guowen Hu 1, * , Qing Yang 2 , Pei Zhang 1 , Wei Kuang 1 , Xingen Zhu 1 , Lei Wu 1 1 Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China 2 Department of Respiratory Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China * These authors have contributed equally to this work Correspondence to: Lei Wu, email: doctorleiming@163.com Xingen Zhu, email: Zhuxg1965@126.com Keywords: qRT-PCR, quantitative real-time PCR; lncRNA, long non-coding RNA (lncRNAs); CCK-8, cell counting kit-8 Received: September 14, 2016 Accepted: October 14, 2016 Published: November 09, 2016 ABSTRACT Long non-coding RNA colon cancer-associated transcript 2 (CCAT2) is commonly investigated in a number of cancers. However, little is known of its expression and biological function in glioma biology. In the current study, we used quantitative real-time PCR (qRT-PCR) to determine the expression of CCAT2 in glioma tissues. We found that expression of CCAT2 was up-regulated in glioma tissues and significantly correlated with the advanced tumor stage (III/IV). Functional assays in vitro and in vivo demonstrated that knockdown of CCAT2 could inhibit proliferation, cell cycle progression and migration of glioma cells. Further analysis indicated the effect of CCAT2 knockdown on glioma cell phenotype through inhibiting Wnt/β-catenin signal pathway activity. Thus, our study provides evidence that CCAT2 may function as a potential biomarker for glioma.

A series of novel arylpiperazine derivatives was synthesized. The in vitro cytotoxic activities of all synthesized compounds against three human prostate cancer cell lines (PC-3, LNCaP, and DU145) were evaluated by a CCK-8 assay. Compounds 9 and 15 exhibited strong cytotoxic activities against LNCaP cells (IC50 < 5 μM), and compound 8 (IC50 = 8.25 μM) possessed the most potent activity against DU145 cells. However, these compounds also exhibited cytotoxicity towards human epithelial prostate normal cells RWPE-1. The structure–activity relationship (SAR) of these arylpiperazine derivatives was also discussed based on the obtained experimental data.

In isolated guinea-pig ileum (GPI), the κ-opioid acute withdrawal response is under the control of several neuronal signaling systems, including the μ-opioid, the A(1)-adenosine and the CB(1) receptors, which are involved in the inhibitory control of the κ-withdrawal response. After κ-opioid system stimulation, indirect activation of μ-opioid, A(1)-adenosine and CB(1) systems is prevented by the peptide cholecystokinin-8 (CCk-8). In the present study, we have investigated whether the NOP system is also involved in the regulation of the acute κ-withdrawal response. Interestingly, we found that in GPI preparation, the NOP system is not indirectly activated by the κ-opioid receptor stimulation, but instead this system is able by itself to directly regulate the acute κ-withdrawal response. Specifically, our results clearly highlight first the existence of an endogenous tone of the NOP system in GPI, and second that it behaves as a functional anti-opioid system. We also found that, the NOP receptor system is involved in the regulation of the CCk-8-induced contracture intensity, only when in the presence of the κ-opioid receptor stimulation. This effect seems to be regulated by an activation threshold mechanism. In conclusion, the NOP system could act as neuromodulatory system, whose action is strictly related to the modulation of both excitatory and inhibitory neurotransmitters released in GPI enteric nervous system.

In rats bled to invariably fatal haemorrhagic shock (mean arterial pressure = 18-24 mmHg), the prompt and sustained improvement of cardiovascular function, obtained with the i.v. injection of cholecystokinin octapeptide (CCK-8, 20 g/kg) is associated with a massive increase in the volume of residual circulating blood (0.69 +/- 0.12 ml/100 g b.w. in saline-treated rats; 1.61 +/- 0.09 ml/100 g b.w. in CCK-8-treated rats). The number of red cells/mm3 and the % Hb content is the same in CCK-8-treated and in control rats. So, in a condition of severe haemorrhage, otherwise incompatible with survival, the i.v. injection of CCK-8 not only induces an impressive increase in arterial pressure and in circulating blood volume, but also greatly improves tissue oxygenation.

Cholecystokinin octapeptide (CCK-8) (20 micrograms/kg i.v.) and tetracosactide [ACTH-(1-24)] (160 micrograms/kg i.v.) restore blood pressure and allow rats subjected to otherwise invariably fatal acute hemorrhage to survive. Atropine sulphate (2-8 mg/kg i.p.), which crosses the blood-brain barrier, dose-dependently prevents this effect both in the case of ACTH-(1-24) and in that of CCK-8. On the other hand, atropine methyl bromide (2-8 mg/kg i.p.), which does not cross the blood-brain barrier, prevents the effect in the case of CCK-8, but not in that of ACTH-(1-24). These data suggest that a cholinergic mechanism is involved in the anti-shock effect of both ACTH-(1-24) and CCK-8, though the sites of action appear to be in the CNS, in the case of ACTH-(1-24), and outside the CNS, in that of CCK-8.