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Purpose: To investigate the relationship between prognosis of gastric cancer (GC) and the expression of P53, Epidermal growth factor receptor (EGFR), Human epidermal growth factor receptor-2 (HER-2), and Vascular endothelial growth factor (VEGF). Methods: One hundred and forty-seven patients admitted to People's Liberation Army General Hospital (Beijing, China) with diagnosis of locally advanced GC were enrolled in the study. Follow-up data were obtained by outpatient review or telephone follow-up. Expressions of P53, EGFR, HER-2 and VEGF were determined by immunohistochemical staining. The relationship between protein expression, clinico-pathological factors, disease-free survival time (DFS) and overall survival (OS) were analyzed. Results: The expressions of EGER, HER-2, P53 and VEGF in GC were 17.7, 17.0, 41.0 and 55.9%, respectively. The expressions of EGFR and P53 were positively correlated (r = 0.306, p < 0.05), while the expressions of VEGF and HER-2 were negatively correlated (r = -0.2, p < 0.05). The expressions of EGFR, HER-2 and VEGF were not related to the clinico-pathological factors (p > 0.05) while expression of P53 was related only to histological grade (p < 0.05). Univariate analysis showed that OS and DFS were longer (p < 0.05) when P53 was lowly expressed. Multiple-factor analysis revealed that histological grade, infiltration depth and P53 expression were independent factors that influenced DFS. Conclusion: These results indicate that the expression of P53, EGFR, HER2 and VEGF can be used to predict prognosis of GC and screening of patients' benefits from adjuvant chemotherapy. [ABSTRACT FROM AUTHOR]

Recent advances have suggested that long noncoding RNAs (lncRNAs) are differentially expressed in ocular tissues and play a critical role in the pathogenesis of different types of eye diseases. Here, we summarize the functions and mechanisms of known aberrantly-expressed lncRNAs and present a brief overview of relevant reports about lncRNAs in such ocular diseases as glaucoma, proliferative vitreoretinopathy (PVR), diabeticretinopathy (DR), and ocular tumors. We intend to highlight comprehensive studies that provide detailed data about the mechanisms of lncRNAs, their applications as diagnostic or prognostic biomarkers, and their potential therapeutic targets. Although our understanding of lncRNAs is still in its infancy, these examples may provide helpful insights into the methods by which lncRNAs interfere with ocular diseases. [ABSTRACT FROM AUTHOR]

Epigenetics is currently one of the most promising areas of study in the field of biomedical research. Scientists have dedicated their efforts to studying epigenetic mechanisms in cancer for centuries. Additionally, the field has expanded from simply studying DNA methylation to other areas, such as histone modification, non-coding RNA, histone variation, nucleosome location, and chromosome remodeling. In ocular tumors, a large amount of epigenetic exploration has expanded from single genes to the genome-wide level. Most importantly, because epigenetic changes are reversible, several epigenetic drugs have been developed for the treatment of cancer. Herein, we review the current understanding of epigenetic mechanisms in ocular tumors, including but not limited to retinoblastoma and uveal melanoma. Furthermore, the development of new pharmacological strategies is summarized. [ABSTRACT FROM AUTHOR]

Increasing evidence suggests that aberrant long non-coding RNAs (lncRNAs) are significantly correlated with the pathogenesis, development and metastasis of cancers. RHPN1 antisense RNA 1 (RHPN1-AS1) is a 2030-bp transcript originating from human chromosome 8q24. However, the role of RHPN1-AS1 in uveal melanoma (UM) remains to be clarified. In this study, we aimed to elucidate the molecular function of RHPN1-AS1 in UM. The RNA levels of RHPN1-AS1 in UM cell lines were examined using the quantitative real-time polymerase chain reaction (qRT-PCR). Short interfering RNAs (siRNAs) were designed to quench RHPN1-AS1 expression, and UM cells stably expressing short hairpin (sh) RHPN1-AS1 were established. Next, the cell proliferation and migration abilities were determined using a colony formation assay and a transwell migration/invasion assay. A tumor xenograft model in nude mice was established to confirm the function of RHPN1-AS1 in vivo. RHPN1-AS1 was significantly upregulated in a number of UM cell lines compared with the normal human retinal pigment epithelium (RPE) cell line. RHPN1-AS1 knockdown significantly inhibited UM cell proliferation and migration in vitro and in vivo. Our data suggest that RHPN1-AS1 could be an oncoRNA in UM, which may serve as a candidate prognostic biomarker and target for new therapies in malignant UM. [ABSTRACT FROM AUTHOR]

MicroRNAs manifest significant functions in brain neural stem cell (NSC) self-renewal and differentiation through the post-transcriptional regulation of neurogenesis genes. Let-7b is expressed in the mammalian brain and regulates NSC proliferation and differentiation by targeting the nuclear receptor TLX, which is an essential regulator of NSC self-renewal. Whether let-7b and TLX act as important regulators in retinal progenitor cell (RPC) proliferation and differentiation remains unknown. Here, our data show that let-7b and TLX play important roles in controlling RPC fate determination in vitro. Let-7b suppresses TLX expression to negatively regulate RPC proliferation and accelerate the neuronal and glial differentiation of RPCs. The overexpression of let-7b downregulates TLX levels in RPCs, leading to reduced RPC proliferation and increased neuronal and glial differentiation, whereas antisense knockdown of let-7b produces robust TLX expression,enhanced RPC proliferation and decreased differentiation. Moreover, the inhibition of endogenous TLX by small interfering RNA suppresses RPC proliferation and promotes RPC differentiation. Furthermore, overexpression of TLX rescues let-7b-induced proliferation deficiency and weakens the RPC differentiation enhancement caused by let-7b alone. These results suggest that let-7b, by forming a negative feedback loop with TLX, provides a novel model to regulate the proliferation and differentiation of retinal progenitors in vitro. [ABSTRACT FROM AUTHOR]