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Cell viability and apoptosis were assessed via MTT and flow cytometry analysis, respectively. Compared with ARPE-19 cells, miR-320a was prominently expressed in retinoblastoma cell lines. TUSC3 was predicted to be a target gene of miR-320a. Compared with ARPE-19 cells, the expression of TUSC3 in retinoblastoma cell lines was reduced. The results of MTT and flow cytometry analysis revealed that overexpression of TUSC3 reduced the viability of retinoblastoma cells and induced apoptosis. Additional analysis indicated that miR-320a inhibitor enhanced the expression of the target gene TUSC3, thereby inhibiting retinoblastoma cell viability and inducing apoptosis. The effects of miR-320a inhibitor on retinoblastoma cells were inhibited by TUSC3-short hairpin RNA. miR-320a regulated the viability and apoptosis of retinoblastoma cells via targeting TUSC3. Therefore, the present study provided a reference for investigating a potential target for the clinical treatment of retinoblastoma.Intracellular calcium (Ca2+) is a critical cell signaling component in gastrointestinal (GI) physiology. Cytosolic calcium ([Ca2+]cyt), as a secondary messenger, controls GI epithelial fluid and ion transport, mucus and neuropeptide secretion, as well as synaptic transmission and motility. The key roles of Ca2+ signaling in other types of secretory cell (including those in the airways and salivary glands) are well known. However, its action in GI epithelial secretion and the underlying molecular mechanisms have remained to be fully elucidated. The present review focused on the role of [Ca2+]cyt in GI epithelial anion secretion. Ca2+ signaling regulates the activities of ion channels and transporters involved in GI epithelial ion and fluid transport, including Cl- channels, Ca2+-activated K+ channels, cystic fibrosis (CF) transmembrane conductance regulator and anion/HCO3- exchangers. Previous studies by the current researchers have focused on this field over several years, providing solid evidence that Ca2+ signaling has an important role in the regulation of GI epithelial anion secretion and uncovering underlying molecular mechanisms. The present review is largely based on previous studies by the current researchers and provides an overview of the currently known molecular mechanisms of GI epithelial anion secretion with an emphasis on Ca2+-mediated ion secretion and its dysregulation in GI disorders. In addition, previous studies by the current researchers demonstrated that different regulatory mechanisms are in place for GI epithelial HCO3- and Cl- secretion. An increased understanding of the roles of Ca2+ signaling and its targets in GI anion secretion may lead to the development of novel strategies to inhibit GI diseases, including the enhancement of fluid secretion in CF and protection of the GI mucosa in ulcer diseases.The human ubiquitin protein ligase E3 component N-recognin 5 (UBR5) gene, which is localized to chromosome 8q22, encodes an ~10 kb mRNA and a >300 kDa protein, which can be detected in a number of cell types. UBR5 is implicated in several types of cancer, including ovarian cancer, gallbladder cancer and lymphoma; however, its role in gastric cancer is not completely understood. In the present study, the expression levels of UBR5 in human gastric cancer tissues and cell lines were examined via immunohistochemistry, reverse transcription-quantitative PCR analysis and western blotting. Furthermore, the association between UBR5 expression and clinicopathological characteristics, as well as the prognosis of patients with gastric cancer, were examined. In addition, the role of UBR5 in gastric cancer cell proliferation, invasion and migration was investigated by conducting MTS, Transwell and wound healing assays, respectively. The results indicated that the mRNA and protein expression levels of UBR5 were significantly increased in gastric cancer tissues compared with para-carcinoma tissues. High UBR5 expression levels were significantly associated with larger tumor size, advanced TNM stage and lymph node metastasis. In addition, high UBR5 expression indicated a poor prognosis in patients with gastric cancer. Furthermore, in vitro experiments demonstrated that UBR5 knockdown was associated with reduced HGC-27 gastric cancer cell proliferation, invasion and migration compared with the small interfering RNA control group. Therefore, the results indicated that UBR5 may serve a key role in gastric cancer, indicating that UBR5 may also serve as an important prognostic biomarker.Reflectance confocal microscopy (RCM) is a non-invasive tool that provides real-time microscopic images and relatively high-resolution tissue images. This technique provides a link between clinical examination and histopathology. SP-13786 RCM has been used to detect skin diseases and has also recently been applied to diseases of the oral mucosa. The present study aimed to explore the features of oral lichen planus (OLP) using RCM. A total of 47 patients with OLP exhibiting a reticular pattern, were included in the present study. The lesion sites and healthy adjacent sites were examined using in vivo RCM, with the lesion being histopathologically confirmed after RCM examination. The confocal images were reviewed, and the features were described. Sensitivity and specificity analysis of the RCM features was also performed. RCM examination presented parakeratosis, acanthosis and connective tissue papillae disappearance, with the presence of large melanocytes and roundish inflammatory cell infiltration, as well as dilated vessels in the lesion tissue. The sensitivity and specificity of OLP for dorsal tongue lesions were not as satisfactory as those on other sites. The results implied that RCM may be a promising technique to detect OLP non-invasively in vivo.The present study aimed to investigate the effects of mechanical stretch and lipopolysaccharides (LPS) on the expression of transforming growth factor-β1 (TGF-β1) and collagen and viscoelasticity in human embryonic MRC-5 lung fibroblasts cultured in vitro and to assess the mechanisms of ARDS-associated ventilator-induced lung injury using an in vitro model. Human embryonic MRC-5 lung fibroblasts were treated with different concentrations of LPS to establish an acute respiratory distress syndrome (ARDS) cell injury model, followed by further culture under different mechanical stretch amplitudes using the Flexcell system to establish a cellular mechanical damage model. The proliferation of MRC-5 cells and the protein and gene expression levels of TGF-β1 and collagen were detected by flow cytometry, ELISA and reverse transcription-quantitative PCR, respectively. As the concentration of LPS increased, the proliferation activity of MRC-5 cells gradually decreased. Low concentrations of LPS led to upregulation of the secretion levels of TGF-β1 and collagen I and the expression of their mRNA, TGF-β1 mRNA and collagen type 1, α1.