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Objective Exploring the influence of rapamycin on the progressing of hepatocellular carcinoma(HCC) in H-ras 12V transgenic mice. Methods The expression level of miRNA in liver tissue and peritumor tissue of transgenic mice was detected by high-throughput sequencing of miRNAs. Treatment of transgenic mice with rapamycin and the changes of tumor morphology were detected. The miR-183 expression levels were detected by RT-qPCR. The protein expression levels of mTOR, ERK and PDCD4, the downstream target gene of miR-183, were detected by Western blot. Results Compared with the peritumor tissue, the miR-183 expression in hepatocellular carcinoma tissue was increased significantly (P＜0.01). The protein expression levels of PDCD4 were decreased significantly(P＜0.05). Compared with the control group, after intervention with rapamycin, the counting of liver tumors decreased significantly(P＜0.05). The liver co-efficient decreased significantly(P＜0.05). The ERK phosphorylation increased significantly (P＜0.05). The miR-183 expression was decreased significantly (P＜0.05). The protein level of PDCD4 increased significantly (P＜0.05). Conclusions Rapamycin can alleviate hepatocellular carcinoma progression in H-ras 12V transgenic mice.

Copyright of Basic & Clinical Medicine is the property of Editorial Office of Basic & Clinical Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the protective effect of β-caryophyllene (BCP) against ischemic stroke injury in mice and clarify whether such protective effects are associated with miR-183 and nuclear factor-κB (NF-κB) expression. Methods Ninety male C57BL/6 mice were randomized equally into 3 groups, namely the sham-operated group, ischemia-reperfusion (I/R) model group, and BCP (72 mg/kg) pretreatment group. The mice in the latter 2 groups were subjected to middle cerebral artery occlusion for 60 min followed by reperfusion for 24 h. The neurological deficits and infarct volume of the mice were measured, and the pathological changes in the brain tissues were observed using HE and Nissl staining. The expression of miR-183, NF-κB, p-NF-κB, interleukin-1β (IL-1β), and IL-6 in the brain were detected, and the targeting relationship between miR-183 and NF-κB was determined. In the in vitro experiment, the cortical neurons isolated from the brain of neonatal mice were divided into normal group, oxygen-glucose deprivation (OGD) group, and OGD group with 10 μmol/L BCP pretreatment. Immunofluorescence assay was employed for morphological observation of the neurons, and the cell injury was assessed with lactate dehydrogenase (LDH) leakage assay. The expression levels of miR-183, IL-1β, IL-6 and NF-κB in the neurons were measured. Results In the mouse models of ischemic stroke, BCP pretreatment significantly improved neurologic deficit score, reduced the infarct volume, lessened pathological changes of the brain tissue, and decreased the number of Nissl-positive cells in the cortex (P < 0.05). BCP pretreatment significantly upregulated the expression of miR-183 in the brain tissues of the mice (P < 0.05). In the in vitro experiment, BCP pretreatment produced obvious protective effect on neurons and significantly lowered neuronal death rate following OGD (P < 0.05). BCP treatment significantly upregulated the expression of miR-183, inhibited NF-κB activation and lowered the expressions of inflammatory factors in the neurons (P < 0.05). Conclusion BCP protects the brain tissues against ischemic stroke injury by upregulating the expression of miR-183, which inhibits NF-κB activation and lowers the release of inflammatory factors to alleviate inflammation in the brain.

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To study the expression and diagnostic value of plasma miR-145 and miR-183 in children with lupus nephritis (LN). Methods A total of 92 children with LN who were admitted from January 2016 to May 2019 were enrolled as the LN group, among whom 17 had type II LN, 15 had type III LN, 36 had type IV LN, 18 had type V LN, and 6 had type VI LN. Forty healthy children who underwent physical examination were enrolled as the healthy control group. According to Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), the 92 children with LN were further divided into a stable LN group with 34 children (SLEDAI score <10) and an active LN group with 58 children (SLEDAI score ≥10). RT-PCR was used to measure the expression of miR-145 and miR-183 in plasma. The receiver operating characteristic (ROC) curve was used to analyze the value of plasma miR-145, miR-183, and anti-dsDNA antibody in the diagnosis of LN. Pearson correlation analysis was used to investigate the correlation of the expression levels of miR-145 and miR-183 in plasma with laboratory markers. Results The LN, active LN, and stable LN groups had significantly higher levels of anti-dsDNA antibody, C-reactive protein, serum creatinine (Scr), and blood urea nitrogen (BUN) than the control group (P<0.05). The active LN group had significantly higher SLEDAI score, anti-dsDNA antibody, Scr, and BUN than the stable LN group (P<0.05). The LN, active LN, and stable LN groups had significantly lower levels of complement C3, complement C4, and serum albumin (Alb) than the control group (P<0.05). The active LN group had a significantly lower level of Alb than the stable LN group (P<0.05). The LN, active LN, and stable LN groups had significantly lower plasma levels of miR-145 and miR-183 than the control group (P<0.01). The active LN group had significantly lower plasma levels of miR-145 and miR-183 than the stable LN group (P<0.01). The children with difference types of LN had significantly lower plasma levels of miR-145 and miR-183 than the control group (P<0.01), and the type V-VI group and the type IV group had significantly lower plasma levels of miR-145 and miR-183 than the type II-III group (P<0.01). The ROC curve analysis showed that the optimal cut-off values of plasma miR-145, miR-183, and anti-dsDNA antibody were 1.05, 0.62, and 186.30 IU/mL respectively, in the diagnosis of LN, and the combination of these three indices had the largest area under the ROC curve of 0.896 (95%CI: 0.835-0.955), with a sensitivity of 90.5% and a specificity of 84.2%. In the children with LN, the plasma levels of miR-145 and miR- 183 were negatively correlated with SLEDAI score, anti-dsDNA antibody, Scr, and BUN (P<0.05) and were positively correlated with complement C3, complement C4, and Alb (P<0.05). Conclusions There are significant reductions in the expression levels of miR-145 and miR-183 in plasma in children with LN, which are correlated with the activity level and pathological typing of LN. Combined measurement of miR-145, miR-183, and anti-dsDNA antibody has a high value in the diagnosis of LN. [ABSTRACT FROM AUTHOR]

Objective · To evaluate level of miR-183 in peripheral blood of the patients with gastric cancer for diagnosis and prognosis. Methods · Quantitative real-time PCR was used to detect the miR-183 levels in sera of 76 cases of gastric cancer patients and 26 cases of normal control at the same term. The correlations of miR-183 levels with clinicopathological features and clinical prognosis were analyzed. Results · The significantly higher levels of miR-183 were observed in the sera of gastric cancer patients (4.798±0.267 vs 0.904±0.067, P=0.000) as compared with those in the corresponding control group. Up-regulation of miR-183 was associated with invasion depth, positive lymph node or distant metastasis, and advanced clinical stage in gastric cancer patients (P<0.05), but not associated with age, sex, and degree of tumor differentiation (P>0.05). ROC curve analysis showed that the AUC value of miR-183 in the prediction of gastric cancer was 0.978 (95% CI 0.955-1.001) with sensitivity of 93.42% and specificity of 92.31%. In the prediction of metastasis (lymph node metastasis or distant metastasis), the AUC value was 0.643 (95% CI 0.507-0.780) with sensitivity of 67.31% and specificity of 58.33%. Conclusion · The high level of miR-183 in serum is associated with gastric cancer development, its clinicopathological features and patient’s clinical prognosis. It may be used as a potential diagnostic bio-marker and a prognostic predictor in the patients with gastric cancer. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the effect of miR-183 on the cell proliferation in SW1990 pancreatic cancer cell line by targeting programmed cell death factor 4(PDCD4)., Methods: The SW1990 pancreatic cancer cells were transfected with miR-183 mimics and inhibitors at different concentrations, the alteration of PDCD4 levels was observed at specific concentrations by qPCR and Western blot. The cellular proliferation of transfected cells was determined by MTT assay. The distribution of cell cycle and apoptosis was examined by flow cytometry (FCM) and Hoechst 33258 staining. The expression of B-cell lymphoma(bcl-2) was evaluated by Western blot., Results: The miR-183 mimic and inhibitor (at concentrations of 50 nmol/L or 150 nmol/L) showed significantly increasing or decreasing effects on the levels of miR -183 respectively. The expression of PDCD4 was downregulated in the cells transfected with miR-183 mimics, while significantly upregulated in the cells treated with miR-183 inhibitors. Western blot showed that miR-183 inhibitors resulted in a marked decrease in the expression levels of bcl-2. The growth of SW1990 cells was obviously inhibited after anti-miR-183 treatment, while an increase of apoptosis cells proportion and cell cycle G₀/G₁ arrest were observed after miR-183 inhibitors transfection., Conclusions: The miR-183 inhibitors could restrain cell proliferation, promote cell apoptosis and increase G₀/G₁ arrest in SW1990 pancreatic cancer cells, which may be possibly through targeting PDCD4.