Purpose It is known that microRNAs (miRNAs) are a class of small, noncoding RNAs that act as key regulators in various physiological and pathological processes. However, the regulatory mechanisms involving miRNAs in retinoblastoma (RB) remain largely unknown. The miRNA miR-125b is dysregulated in various human cancers such as breast cancer, human hepatocellular carcinoma, ovarian cancer, and colorectal cancer. However, the significance of miR-125b in RB has not been sufficiently investigated. Our objective was to explore the role of the miR-125b in RB. Methods In this study, we measured miR-125b levels using real-time polymerase chain reaction in human RB cell lines, including HXO-Rb44, Y79, SO-RB50, and the normal human retinal pigment epithelial cell line ARPE-19; a total of 38 pairs of primary RB tissues and adjacent noncancerous tissues were also measured. In addition, overexpression of miR-125b in RB cell lines was performed to determine the role of miR-125b in RB. Results We found that miR-125b is significantly upregulated in RB, and closely associated with tumor cell proliferation and apoptosis. In addition, overexpression of miR-125b apparently promotes RB cell proliferation and migration in vitro. Gain-offunction in vitro experiments further showed that the miR-125b mimic significantly suppressed RB cell apoptosis. A subsequent dual-luciferase reporter assay identified the suppressor gene DRAM2 as direct target of miR-125b.Conclusions Our data collectively demonstrate that miR-125b is a suppressor gene miRNA that can promote RB cell proliferation and migration by downregulating the suppressor gene DRAM2, indicating that miR-125b may represent a new potential diagnostic and therapeutic target for RB treatment.

Soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins are a large protein complex that is involved in the membrane fusion in vesicle trafficking, cell growth, cytokinesis, membrane repair, and synaptic transmission. As one of the SNARE proteins, SEC22B functions in membrane fusion of vesicle trafficking between the endoplasmic reticulum and the Golgi apparatus, antigen cross-presentation, secretory autophagy, and other biological processes. However, apart from not being SNARE proteins, there is little knowledge known about its two homologs (SEC22A and SEC22C). SEC22B alterations have been reported in many human diseases, especially, many mutations of SEC22B in human cancers have been detected. In this review, we will introduce the specific functions of SEC22B, and summarize the researches about SEC22B in human cancers and other diseases. These findings have laid the foundation for further studies to clarify the exact mechanism of SEC22B in the pathological process and to seek new therapeutic targets and better treatment strategies.

Nucleotide metabolism is the driving force of cell proliferation, and thymidylate synthase (TYMS) catalyzes a rate‐limiting step in the initial synthesis of nucleotides. Previous studies reported that TYMS activity significantly affected the proliferation of tumour cells. However, the diagnostic and prognostic significance of TYMS expression in breast cancer remains unclear. Here, we used the Breast Cancer Integrative Platform (BCIP) to investigate the relationship between progression and prognosis of breast cancer with TYMS expression, and then verified the database analysis using immunohistochemical staining. Our results indicated TYMS expression was greater in breast cancer than adjacent normal tissues and greater in triple‐negative breast cancer (TNBC) than non‐TNBC tissues. TYMS expression also had significant positive correlations with histological grade, tumour size, and ER negativity, and PR negativity. The increased copy number of the TYMS gene appears to be the reason for its upregulation in breast cancer. Breast cancer patients with higher TYMS expression had poorer prognosis. Our data suggest that TYMS has potential use as a diagnostic and prognostic marker for breast cancer patients.

Background: It has been a decade since the complex fractionated atrial electrograms (CFAEs) were first established following the publication of Nademanee's standards. However, the status and focus of CFAE research are unclear, as is the efficacy of additional CFAE ablation in atrial fibrillation (AF). This literature review and metaanalysis were designed to determine the status of CFAE research and the efficacy and complications of CFAE ablation alone, pulmonary vein isolation (PVI) alone and PVI plus CFAE ablation in AF. Methods: With the assistance from reference librarians and investigators trained in systematic review, we conducted a literature search of MEDLINE (via PubMed), Embase, the Cochrane Library, ScienceDirect, Wiley Blackwell and Web of Knowledge, using "complex fractionated atrial electrograms" for MeSH and keyword search. Results: The literature on CFAEs increased from 2007, mainly focusing on mapping studies, with mechanism studies increasing significantly from 2012. Fifteen trials with 1525 patients were qualified for our meta-analysis. Success rates were as follows. Overall (P b 0.001): CFAE ablation alone, 23.5-26.2%; PVI, 64.7%; PVI plus CFAE ablation, 67.0%. Single ablation: PVI, 60.4%; PVI plus CFAEs, 68.8% (OR 1.53, 95% CI 1.07-2.20, P = 0.02). Reablation: PVI, 69.0%; PVI plus CFAEs, 77.2% (OR 1.54, 95% CI 1.06-2.24, P = 0.02). Paroxysmal AF: PVI, 76.7%; PVI plus CFAEs, 79.1% (OR 1.20, 95% CI 0.79-1.81, P = 0.39). Persistent or permanent AF: PVI, 47.9%; PVI plus CFAEs, 58.7% (OR = 1.59, 95% CI 1.13-2.24, P = 0.008). Complication rates: PVI, 2.6%; PVI plus CFAEs, 3.4% (OR 1.22, 95% CI 0.58-2.57, P = 0.61). Conclusions: In the literature, CFAE mapping studies preceded mechanism studies. CFAE ablation alone is insufficient for the treatment of AF. Additional CFAE ablation after adequate PVI or PVI plus linear ablation improves the outcome of single ablation and re-ablation without increasing complications, especially in persistent or permanent AF. There are insufficient data to support a similar improvement in paroxysmal AF or inducible AF after PVI for paroxysmal AF.