We have previously shown that the integrin  6 is neoexpressed in invasive oral squamous cell carcinoma (SCC) and is correlated with oral tumor progression. However, the mechanism by which the integrin  6 promotes oral tumor progression is not well understood. The purpose of the present study was to determine whether integrin  6 signaling activates Fyn and thus promotes oral squamous cell carcinoma progression. We analyzed the integrin  6 signaling complex and investigated the function of these signaling molecules in oral SCC cells. We found that, upon ligation of the integrin  6 with fibronectin,  6 complexed with Fyn and activated it. The activation of Fyn recruited and activated focal adhesion kinase to this complex. This complex was necessary to activate Shc and to couple  6 signaling to the Raf-ERK/MAPK pathway. This pathway transcriptionally activated the matrix metalloproteinase-3 gene and promoted oral SCC cell proliferation and experimental metastasis in vivo. These findings indicate that integrin  6 signaling activates Fyn and thus promotes oral cancer progression.
The Effect of Occupational Exposure to Metals on the Nervous System Function in Welders:Xianliang WANG, et al. MOE Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, China-We explored the relationship between metals exposure and nervous impairment in welders. The metals exposure of 82 welders and 51 operators were evaluated for blood Pb, Cd and Mn by atomic absorption spectrometry, and the nervous system impairment was evaluated with the n e u r o b e h a v i o r a l c o r e t e s t b a t t e r y a n d electromyography. Pb (geometric mean: 117.31 µg/L; range: 0.5-327.6 µg/L) and Cd (geometric mean: 3.54 µg/L; range: 0.2-12.5 µg/L) in welders were significantly higher than those in operators. Welders had higher prevalence of nervous system symptoms and worse standard scores of 8 items such as depressiondejection than operators. Significant difference of nervous performance in welders only existed in different concentration groups of Pb and Mn. The performances of fatigue-inertia and some others had negative correlations with Pb and digit span with Mn. Therefore, the nervous system impairment in welders could be attributed to occupational exposure of Pb and Mn, but not Cd, concomitantly. 1) found increased symptoms in welders were related to decreased scores on tasks measuring verbal learning, visuomotor abilities, visuospatial abilities, information processing and motor efficiency. Another study revealed Mn exposure within the range of 0.01-2.67 mg/m 3 could induce subclinical effects on the nervous system 2) , but only the time for welding or the air concentration of Mn was calculated without biological sample collection in these studies.Pb is also a common neurotoxic agent besides Mn. Cd can cause adverse effects on multiple organs, especially the kidney. These metals can be easily absorbed into the body through the respiratory tract. The cases of serious damage to the nervous system have become rare due to the efforts of health promotion among welders. Due to the variability of work settings for welders, it is almost impossible to assess the exposure to neurotoxic metals by means of one universal indicator. Therefore, it is optimal to resort the co-measurement of several metals in biological samples and examination of the performance of the nervous system with neurobehavioral methods in welders due to the objective and sensitivity of neurobehavioral examination and electroneurophysiological detection.To explore the effects of welding on the nervous system among welders and the relationship between Pb, Cd and Mn in blood and the central and peripheral nervous systems functions, a cross-sectional study was carried out in Hefei, China. Methods SubjectsThe subjects in this study were from two vehicle manufactures located next to each other in a suburb of Hefei, a central city of Anhui province in China. Workers welding longer than 6 months continuously by cluster sampling were subjects of the study. A control group
Results from a meta-analysis of aggregated data provoked a new analysis using individual data on the neuropsychological performance of occupationally exposed workers. Data from eight studies examining 579 exposed and 433 reference participants were included, 28 performance variables analyzed. The performance scores were adjusted for well-known individual-level covariates; the influence of possible, but unknown study-level covariates was attenuated by means of a z-normalization. Associations between performance and exposure were estimated by ANOVAs and ANCOVAs, the latter representing multi-level models. Four cognitive and motor performance variables each indicated significantly lower performances of exposed individuals when confounding was considered; slowed motor performances and deficits in attention and short-term memory were found. Performance on a single test was significantly related to the biomarker manganese in blood. The outcomes on susceptibility were weak. The slowing of responses was the most distinct feature of performances of exposed workers. It remains unclear, whether this result is related to the employed tests or provides important information about early stages of the neurotoxic impairment. More specific cognitive tests need to be employed to answer this question. The lack of dose–response relationships was related to features of the biomarker: it does not reflect the Mn in brain responsible for changes in performances.
MicroRNA-126 (miR-126) has previously been reported to be downregulated in various types of cancer; however, at present, there are no studies of miR‑126 in human thyroid cancer. The present study aimed to determine the expression and effects of miR‑126 on thyroid cancer. The expression levels of miR‑126 were detected in human thyroid cancer tissues, matched normal adjacent tissues and human thyroid cancer cell lines using quantitative polymerase chain reaction. In addition, post‑transfection of human thyroid cancer cells with miR‑126 mimics, cell proliferation, migration and invasion assays, western blot analysis and luciferase assays were conducted. The results demonstrated that miR‑126 was downregulated in thyroid cancer tissues and cells. Furthermore, upregulation of miR‑126 inhibited cell proliferation, migration and invasion in thyroid cancer cells. The present study also provided evidence suggesting that miR‑126 may directly target C‑X‑C chemokine receptor type 4 (CXCR4) in thyroid cancer. These results indicated that miR‑126 may be investigated as a target for the treatment of thyroid cancer.
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