Background: Neuroblastoma (NB) is the most common solid extracranial tumor in children. However, the molecular mechanism and progression of NB is largely unknown, and unfortunately, the prognosis is poor. Src-associated in mitosis with a molecular weight of 68 kDa (Sam68) is associated with carcinogenesis and neurogenesis. The present study aimed to investigate the clinical and prognostic significance of Sam68 in NB.
Methods: The expression of Sam68 in immortalized normal epithelial cells, NB cell lines, and in four cases of paired NB tissue and adjacent normal tissue from the same patient was examined using Western blotting, reverse transcription-polymerase chain reaction (PCR) and real-time reverse transcription-PCR. The proliferation of NB cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Furthermore, Sam68 protein expression was analyzed in 90 NB cases characterized as clinicopathological using immunohistochemistry. Statistical analyses were applied to evaluate the diagnostic value and associations of Sam68 with clinical parameters.
Results: Western blotting and reverse transcription-PCR showed that the expression level of Sam68 was markedly higher in NB cell lines than in the immortalized normal epithelial cells at both messenger RNA and protein levels. The MTT assay revealed that Sam68 expression supported proliferation of NB cells. Sam68 expression levels were significantly up-regulated in tumor tissues in comparison to the matched adjacent normal tissues from the same patient. Sam68 protein level was positively correlated with clinical stage (P<0.001), tumor histology (P<0.001), and distant metastasis (P=0.029). Patients with higher Sam68 expression had shorter overall survival time, whereas those with lower tumor Sam68 expression had longer survival time.
Conclusion: Our results suggest that Sam68 expression is associated with neuroblastoma progression and may represent a novel and valuable predictor for prognostic evaluation of neuroblastoma patients.
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http://dx.doi.org/10.2147/OTT.S52643 | DOI Listing |
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Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Youseong-Gu, Daejeon, 34141, Republic of Korea.
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Department of Medical Biochemistry, Molecular Biology and Immunology, School of Medicine, University of Seville, 41009 Seville, Spain.
Src‑associated in mitosis 68 kDa protein (Sam68) is a protein encoded by the heteronuclear ribonucleoprotein particle K homology (KH) single domain‑containing, RNA‑binding, signal transduction‑associated protein 1 (known as ) gene in humans. This protein contains binding sites for critical components in a variety of cellular processes, including the regulation of gene expression, RNA processing and cell signaling. Thus, Sam68 may play a role in a variety of diseases, including cancer.
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Edinburgh Medical School, UK Dementia Research Institute at the University of Edinburgh, Edinburgh, United Kingdom.
Rodent studies have shown that alternative splicing in neurons plays important roles in development and maturity, and is regulatable by signals such as electrical activity. However, rodent-human similarities are less well explored. We compared basal and activity-dependent exon splicing in cortical-patterned human ESC-derived neurons with that in cortical mouse ESC-derived neurons, primary mouse cortical neurons at two developmental stages, and mouse hippocampal neurons, focussing on conserved orthologous exons.
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Department of Medical Biochemistry, Molecular Biology and Immunology, University of Seville Medical School, 41009 Seville, Spain.
Obesity is frequently accompanied by non-alcoholic fatty liver disease (NAFLD). These two diseases are associated with altered lipid metabolism, in which reverse cholesterol transport (LXRα/ABCA1/ABCG1) and leptin response (leptin receptor (Ob-Rb)/Sam68) are involved. The two pathways were evaluated in peripheral blood mononuclear cells (PBMCs) from 86 patients with morbid obesity (MO) before and six months after Roux-en-Y gastric bypass (RYGB) and 38 non-obese subjects.
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