Abstract. miR-200a suppresses tumor development and progression; however, its role in tumor growth and metastasis of hepatocellular carcinoma (HCC) and the underlying mechanism have not been elucidated. In the present study, we identified that miR-200a was markedly downregulated in HCC and exerted suppressive effects on tumor cell growth and metastasis. We identified that miR-200a suppressed tumor growth and metastasis by directly targeting MACC1. In addition, HCC patients with low miR-200a expression had significantly worse prognosis than those with high expression of miR-200a. These findings suggest that miR200a may be recognized as a novel potential biomarker to predict the survival of patients with HCCs following liver transplantation.
BackgroundThe objective of this study was to evaluate the feasibility, safety, and potential benefits of laparoscopic gastrectomy (LG) comparing with open gastrectomy (OG) in elderly population.MethodsStudies comparing LG with OG for elderly population with gastric cancer, published between January 1994 and July 2015, were identified in the PubMed, Embase, and ISI Web of Science databases. Operative outcomes (intraoperative blood loss, operative time, and the number of lymph nodes harvested) and postoperative outcomes (time to first ambulation, time to first flatus, time to first oral intake, postoperative hospital stay, postoperative morbidity) were included and analyzed. The Newcastle-Ottawa Scale was used to assess the quality of the pooled study. A funnel plot was used to evaluate the publication bias.ResultsSeven studies totaling 845 patients were included in the meta-analysis. LG in comparison to OG showed less intraoperative blood loss (weighted mean difference (WMD) −127.47; 95 % confidence interval (CI) −202.79 to −52.16; P < 0.01), earlier time to first ambulation (WMD −2.07; 95 % CI −2.84 to −1.30; P < 0.01), first flatus (WMD −1.04; 95 % CI −1.45 to −0.63; P < 0.01), and oral intake (WMD −0.94; 95 % CI −1.11 to −0.77; P < 0.01), postoperative hospital stay (WMD −5.26; 95 % CI −7.58 to −2.93; P < 0.01), lower overall postoperative complication rate (odd ratio (OR) 0.39; 95 % CI 0.28 to 0.55; P < 0.01), less surgical complications (OR 0.47; 95 % CI 0.32 to 0.69; P < 0.01), medical complication (OR 0.35; 95 % CI 0.22 to 0.56; P < 0.01), incisional complication (OR 0.40; 95 % CI 0.19 to 0.85; P = 0.02), and pulmonary infection (OR 0.49; 95 % CI 0.26 to 0.93; P = 0.03). No significant differences were observed between LG and OG for the number of harvested lymph nodes. However, LG had longer operative times (WMD 15.73; 95 % CI 6.23 to 25.23; P < 0.01).ConclusionsLG is a feasible and safe approach for elderly patients with gastric cancer. Compared with OG, LG has less blood loss, faster postoperative recovery, and reduced postoperative morbidity.
Toxoplasma gondii is an obligate intracellular parasite, which is responsible for a widely distributed zoonosis. Effective vaccines against toxoplasmosis are necessary to protect the public health. The aim of this study is to evaluate the immune efficacy of DNA vaccines encoding TgMIC5 and TgMIC16 genes against T. gondii infection. The recombinant plasmid pVAX-MIC5 and pVAX-MIC16 were constructed and injected intramuscularly in mice. The specific immune responses and protection against challenge with T. gondii RH tachyzoites were evaluated by measuring the cytokine levels, serum antibody concentrations, lymphocyte proliferation, lymphocyte populations, and the survival time. The protection against challenge with the T. gondii RH tchyzoites and PRU cysts was examined by evaluation of the reduction in the brain cyst burden. The results indicated that immunized mice showed significantly increased levels of IgG, IFN-γ, IL-2, IL-12p70, and IL-12p40 and percentages of CD4+ and CD8+ T cells. Additionally, vaccination prolonged the mouse survival time and reduced brain cysts compared with controls. Mouse groups immunized with a two-gene cocktail of pVAX-MIC5 + pVAX-MIC16 were more protected than mouse groups immunized with a single gene of pVAX-MIC5 or pVAX-MIC16. These results demonstrate that TgMIC5 and TgMIC16 induce effective immunity against toxoplasmosis and may serve as a good vaccine candidate against T. gondii infection.
Liver fibrosis is a wound-healing response and the activation of the hepatic stellate cell (HSC) is the core of hepatic fibrosis. MicroRNAs (miRNAs) participate in the development of fibrosis. It is reported that histone deacetylases (HDAC2) tyrosine phosphorylation by cellular-Abelsongene (c-Abl) induces malignant growth of cells. Here, we investigated the effect of miR-122-5p on the proliferation and apoptosis of HSCs. Normal human HSC line LX-2 and LX-2 cells stimulated by transforming growth factor (TGF)-β1 for 24 h were cultured and assigned into the blank group and the TGF-β1 group. The miR-122-5p inhibitor and its negative control were transfected into LX-2 cells and miR-122-5p mimic and its negative control were transfected into LX-2 cells stimulated by TGF-β1. The result showed that miR-122-5p expression was decreased in TGF-β1-stimulated LX-2 cells. miR-122-5p overexpression reduced the mRNA and protein levels of collagen I and α-smooth muscle actin, inhibited cell proliferation, and accelerated cell apoptosis. miR-122-5p targeted c-Abl. Meanwhile, miR-122-5p overexpression inhibited HSC activation by suppressing the c-Abl/HDAC2 pathway. In summary, miR-122-5p overexpression exerted anti-fibrosis effect and inhibited HSC activation by suppressing the c-Abl/HDAC2 pathway.
Background Hepatocellular carcinoma (HCC) is the most common malignancy in the elderly worldwide, but it is also common among younger individuals in areas with endemic hepatitis B virus infection. The differences in long-term oncological prognosis of young versus elderly patients after R0 liver resection for HCC were explored in this study. Methods Using a Chinese multicentre database, consecutive patients who underwent R0 liver resection for HCC between 2007 and 2019 were analysed retrospectively. After excluding middle-aged (36–69 years old) patients, overall survival (OS), cancer-specific survival (CSS), and recurrence were compared between young (35 years or younger) and elderly (70 years or older) patients using propensity score matching (PSM). Results Among 531 enrolled patients, there were 192 (36.2 per cent) and 339 (63.8 per cent) patients categorized as young and elderly respectively. PSM created 140 pairs of matched patients. In the PSM cohort, 5-year OS was comparable for young versus elderly patients (51.7 versus 52.3 per cent, P = 0.533). Young patients, however, had a higher 5-year cumulative recurrence rate (62.1 versus 51.6 per cent, P = 0.011) and a worse 5-year CSS rate (54.0 versus 64.3 per cent, P = 0.034) than elderly patients. On multivariable Cox regression analyses, young patient age remained independently associated with an increased recurrence rate (hazard ratio 1.62, P = 0.016) and a decreased CSS rate (hazard ratio 1.69, P = 0.021) compared with older age. Conclusion Following R0 liver resection for HCC, younger patients were at a higher risk of recurrence, and elderly patients had a better CSS rate. Thus, enhanced surveillance for HCC recurrence should be implemented for young patients.
Background. Pancreatic cancer (PC) leads to high human malignancy mortality worldwide. This study explored the role of Astragalus polysaccharide (APS) on human PC PANC-1 cells and its underlying mechanisms. Method. Cell viability, proliferation, apoptosis, invasion, and migration were measured by CCK-8, EdU incorporation, flow cytometry, Transwell, and wound healing assay, respectively. ELISA assay was utilized to detect the IL-1α, IL-4, IL-6, IL-8, and TNF-α levels. The western blot assay was performed to measure the level changes of cell function-related proteins. The transportation of NF-κB P65 protein was detected through immunofluorescence assay. Results. Compared with the control group, APS treatment could significantly inhibit cell proliferation. APS treatment could also suppress cell migration and invasion ability and induce apoptosis and inflammation in PANC-1 cells. Furthermore, APS inhibited the activation of TLR4/NF-κB signaling pathway via suppressing the phosphorylation and transportation of NF-κB P65 into the PANC-1 cell nucleus. Conclusion. APS suppresses PANC-1 cell viability, proliferation, migration, and invasion while inducing inflammation and apoptosis. APS might regulate PC cell motility via downregulating TLR4/NF-κB signaling pathway.
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