Objectives. Breast cancer is the most common malignant tumor among females, and miRNAs have been reported to play an important regulatory role in breast cancer progression. This study aimed to explore the function and underlying molecular mechanism of miR-301b-3p in breast cancer. Methods. Differential analysis and survival analysis were performed based on the data accessed from the TCGA-BRCA dataset for identification of the target miRNA. Bioinformatics analysis was conducted to predict the downstream target gene of the miRNA. Real-time quantitative PCR was carried out to detect the expression of miR-301b-3p and nuclear receptor subfamily 3 group C member 2 (NR3C2). Western blot was used to assess the protein expression of NR3C2. Cell counting kit-8 assay was performed to evaluate the proliferation of breast cancer cells. Transwell assay was conducted to determine the migratory and invasive abilities of breast cancer cells. Dual-luciferase reporter assay was employed to verify the targeting relationship between miR-301b-3p and NR3C2. Results. miR-301b-3p was elevated in breast cancer cell lines and promoted cell proliferation, migration, and invasion in terms of its biological function in breast cancer. NR3C2 was validated as a direct target of miR-301b-3p via bioinformatics analysis and dual-luciferase reporter assay, and NR3C2 was downregulated in breast cancer cell lines. The rescue experiment indicated that NR3C2 was involved in the mechanism by which miR-301b-3p regulated the malignant phenotype of breast cancer cells. Conclusion. The present study revealed for the first time that miR-301b-3p could foster breast cancer cell proliferation, migration, and invasion by targeting NR3C2, unveiling that miR-301b-3p is a novel carcinogen in breast cancer.

Background/Aims: Apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, has been identified as a potential neuroprotectant. In this study, we aimed to investigate the protective effect of apocynin against cobalt chloride (CoCl₂)-induced pheochromocytoma (PC12) cell apoptosis. Methods: The PC12 cell culture was pretreated with apocynin and/or SB203580 (p38 mitogen-activated protein kinase [p38-MAPK] inhibitor) at different time points prior to CoCl₂ incubation. The cell viability, apoptosis rate, DAN damage, and antioxidant activity were detected using cell counting kit-8 (CCK-8), flow cytometry, enzyme-linked immunosorbent assay (ELISA), and comet assay respectively. The protein and mRNA expressions of p38-MAPK and caspase-3 in the cells were measured by qRT-PCR and Western blotting. Results: Apocynin inhibited CoCl₂-mediated apoptosis, reduced oxidative stress, and down-regulated the expression of p38-MAPK and caspase-3. Conclusions: Our findings show that apocynin attenuated CoCl₂-induced apoptosis by potently restraining p38-MAPK-caspase-3 signaling pathway in PC12 cells, suggesting that apocynin may be a potent prophylactic reagent against CoCl₂-mediated PC12 cell apoptosis.

Thyroid cancer (TC) is the most common endocrine malignant disease with a rising morbidity year by year. Accumulating studies have shown that microRNAs (miRNAs) play a regulatory role in the progression of various tumors, but the molecular regulatory mechanism of miR-196a-2 in TC is still unknown. qRT-PCR was employed to measure the expression of miR-196a-2 and NRXN1 mRNA in TC cells, while western blot was used to detect the protein expression of NRXN1. CCK-8, colony formation and flow cytometry assays were used to measure cell proliferation and apoptosis of TC cells. Dual-luciferase reporter gene assay was used to predict and verify the targeted binding relationship between miR-196a-2 and NRXN1. Our study results manifested that miR-196a-2 was dramatically overexpressed in cells of TC, while NRXN1 was lowly expressed. miR-196a-2 could promote cell proliferation and inhibit cell apoptosis of TC. Additionally, miR-196a-2 could also target and inhibit the expression of NRXN1. Silencing NRXN1 could reverse the inhibitory effect of miR-196a-2 downregulation on cell proliferation of TC, as well as the promoting effect on cell apoptosis. In a conclusion, we found that miR-196a-2 could promote cell proliferation and inhibit cell apoptosis of TC by targeting NRXN1. Therefore, miR-196a-2/NRXN1 is potential to be a molecular therapeutic target for TC.

Background: Platelet-to-lymphocyte ratio (PLR) is reported to be related to the outcome of intensive care unit (ICU) patients. However, little is known about their associations with prognosis in newborn patients in neonatal ICU (NICU). The aim of the present study was to investigate the prognostic significance of the PLR for newborn patients in the NICU. Methods: Data on newborn patients in the NICU were extracted from the Multiparameter Intelligent Monitoring in Intensive Care III (MIMIC III) database. The initial PLR value of blood examinations within 24 h was analyzed. Spearman's correlation was used to analyze the association of PLR with the length of hospital and ICU stays. The chi-square test was used to analyze the association of PLR with mortality rate. Multivariable logistic regression was used to determine whether the PLR was an independent prognostic factor of mortality. The area under the receiver operating characteristic (ROC) curve was used to assess the predictive ability of models combining PLR with other variables. Results: In total, 5240 patients were enrolled. PLR was negatively associated with length of hospital stay and ICU stay (hospital stay: ρ = −0.416, p < 0.0001; ICU stay: ρ = −0.442, p < 0.0001). PLR was significantly correlated with hospital mortality (p < 0.0001). Lower PLR was associated with higher hospital mortality (OR = 0.85, 95% CI = 0.75–0.95, p = 0.005) and 90-day mortality (OR = 0.85, 95% CI = 0.76–0.96, p = 0.010). The prognostic predictive ability of models combining PLR with other variables for hospital mortality was good (AUC for Model 1 = 0.804, 95% CI = 0.73–0.88, p < 0.0001; AUC for Model 2 = 0.964, 95% CI = 0.95–0.98, p < 0.0001). Conclusion: PLR is a novel independent risk factor for newborn patients in the NICU.