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PURPOSE: miRNAs can act as oncogenes or tumor suppressors and participate in the development and progression of tumors, thus affecting the prognosis and survival of cancer patients. In this paper, we mainly studied the role of miR-1826 in prostate cancer. PATIENTS AND METHODS: The expression of miR-1826 was studied by quantitative real-time PCR (qRT-PCR). Kaplan-Meier curves were used to analyze the relationship between the expression of miR-1826 and the survival rate of PC patients. Cox regression analysis was used to study the risk factors affecting the prognosis of PC patients. PC cells were transfected with miR-1826 mimic, mimic negative control (mimic NC), miR-1826 inhibitor, or inhibitor NC. The effect of miR-1826 on the proliferation of PC cells was studied by the CCK-8 method and colony formation assay. Transwell assays were used to detect the effect of miR-1826 on the migratory and invasive abilities of tumor cells. RESULTS: The expression of miR-1826 in PC tissues was lower than that in adjacent normal tissues, and that the expression levels of miR-1826 in four PC cell lines were all lower than normal human prostate epithelial cell lines. Patients with low expression of miR-1826 had shorter overall survival compared with those with high expression. The downregulation of miR-1826 promoted PC cell proliferation, migration, and invasion. CONCLUSION: In summary, the low expression of miR-1826 may promote the progression of PC, and the low expression of miR-1826 is also associated with a poor prognosis in PC patients.
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BACKGROUND: This study mainly explored the expression level of LINC-PINT in bladder cancer and its relationship with prognosis. Meanwhile, the effect of LINC-PINT on the biological function of bladder cancer was also explored. METHODS: The expression levels of LINC-PINT and miR-155-5p were detected by qRT-PCR. The prognostic significance of LINC-PINT in bladder cancer was studied by the Kaplan-Meier curve and Log rank test. CCK-8 and Transwell assays were used to analyze the proliferation, migration, and invasion ability. The targeting relationship between LINC-PINT and miR-155-5p was analyzed using bioinformatics and dual-luciferase reporter assays. RESULTS: The expression of LINC-PINT was downregulated in bladder cancer tissues and cell lines, and miR-155-5p showed the opposite trend in bladder cancer tissues. Kaplan-Meier curve proved that the patients with low LINC-PINT expression had a lower five-year survival rate and the Log rank test displayed that LINC-PINT was a prognostic factor of BC. CCK-8 and Transwell results showed that LINC-PINT could inhibit the ability of proliferation, migration, and invasion. LINC-PINT was proved to target miR-155-5p in bladder cancer. Dual-luciferase reporter gene assay showed that the relative luciferase activity of overexpression miR-155-5p co-transfected with LINC-PINT-wt was significantly lower. LINC-PINT was negatively correlated with miR-155-5p. CONCLUSION: LINC-PINT is a potential prognostic marker of bladder cancer, and the up-regulation of Lin-PINT can inhibit the proliferation, invasion, and migration of bladder cancer cells by targeting miR-155-5p.
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BACKGROUND: The aim of this study is to summarize and quantify the current evidence on the therapeutic efficacy of laparoscopic radical nephrectomy (LRN) compared with open radical nephrectomy (ORN) in patients with renal cell carcinoma (RCC) in a meta-analysis. METHODS: Data were collected by searching Pubmed, Embase, Web of Science, and ScienceDirect for reports published up to September 26, 2016. Studies that reported data on comparisons of therapeutic efficacy of LRN and ORN were included. The fixed-effects model was used in this meta-analysis if there was no evidence of heterogeneity; otherwise, the random-effects model was used. RESULTS: Thirty-seven articles were included in the meta-analysis. The meta-analysis showed that the overall mortality was significantly lower in the LRN group than that in the ORN group (odds ratio [OR] =0.77, 95% confidence interval [CI]: 0.62-0.95). However, there was no statistically significant difference in cancer-specific mortality (OR=0.77, 95% CI: 0.55-1.07), local tumor recurrence (OR=0.86, 95% CI: 0.65-1.14), and intraoperative complications (OR=1.27, 95% CI: 0.83-1.94). The risk of postoperative complications was significantly lower in the LRN group (OR=0.71, 95% CI: 0.65-0.78). In addition, LRN has been shown to offer superior perioperative results to ORN, including shorter hospital stay days, time to start oral intake, and convalescence time, and less estimated blood loss, blood transfusion rate, and anesthetic consumption. CONCLUSION: LRN was associated with better surgical outcomes as assessed by overall mortality and postoperative complications compared with ORN. LRN has also been shown to offer superior perioperative results to ORN.
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Tanshinone IIA (T2A), a derivative of phenanthrenequinone and also the major active ingredient of Danshen, has been paid extensive attention as a promising cancer therapy for its potential anti-cancer activities. In this study, the apoptosis and autophagy of human prostate cancer PC-3 cells were observed after 5 µM T2A treatment, as well as their relevance. Mitochondrial-dependent apoptosis was firstly detected through morphological observation and biochemical analysis. Meanwhile, 5 µM T2A successfully triggered the autophagy of PC-3 cells, indicated by increased expression of Beclin1, and LC3 II. Validation experiments were conducted to further consolidate T2A's contribution to autophagy: Pretreatment with autophagy inhibitor 3-methyladenine (3-MA) provided protection against autophagy and enhanced T2A-induced apoptosis. Besides, the apoptosis suppressor z-VAD-fmk failed to facilitate the formation of autophagic vacuoles, which also proved the T2A-induced autophagy independent of apoptosis. Moreover, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) efficiently inhibited the expression of Beclin1, LC3-II, and cleaved caspase-3, which indicated apoptosis and autophagy with dependence on intracellular ROS production. Taken together, these results demonstrated that autophagy is the cytoprotective mechanism in this experimental system, and the ROS resulted from T2A treatment played a critical role in apoptosis and autophagy initiation.
