33 research outputs found

    ECMO survival rate in the different patient subgroups with stratification by cardiogenic shock, APACHE II score, and SAPS II score.

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    <p>ECMO survival rate in the different patient subgroups with stratification by cardiogenic shock, APACHE II score, and SAPS II score.</p

    Additional file 7: of Isocitrate dehydrogenase 1–snail axis dysfunction significantly correlates with breast cancer prognosis and regulates cell invasion ability

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    Figure S3. IDH1 stable knockdown significantly promoted MDA-MB-231 cell motility. (a) The expression levels of IDH1 were examined in two IDH1 stable knockdown MDA-MB-231 cells (shIDH1#1 and shIDH1#2) through western blotting. (b) Invasion ability was assessed using the Transwell assay in MDA-MB-231 cells with IDH1 stable knockdown and a scrambled control. The cell images of the representative experiment are provided. (c) Values were quantified using Ascent software, as detailed. Data are reported as the number of invading cells relative to the control (means Âą standard deviation (SD)). (d) Expression levels of IDH1, snail, slug, twist, and actin were examined in shIDH1#1, shIDH1#2, and the scrambled control through western blotting. (TIFF 3572 kb

    Additional file 9: of Isocitrate dehydrogenase 1–snail axis dysfunction significantly correlates with breast cancer prognosis and regulates cell invasion ability

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    Figure S5. IDH1 knockdown accelerated MCF7 cell proliferation and migration ability. (a) the expression levels of IDH1 were examined in MCF7 cells with siIDH1#1, siIDH1#2, and control transfection through western blotting. (b) A wound healing assay was employed to examine MCF7 cells transfected with siIDH1#1, siIDH1#2, and the scrambled control. (c) The expression levels of IDH1, snail, slug, twist and actin were examined in siIDH1#1, siIDH1#2, and the scrambled control through western blotting. (d) The proliferation assay was performed in MCF-7 cells transfected with the scrambled control, siIDH1#1 and siIDH1#2, respectively. (TIFF 4527 kb

    Expression levels of cleaved caspase-3 and caspase-3 in tumorigenesis and prognosis of oral tongue squamous cell carcinoma

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    <div><p>Apoptosis plays a dual role in cancer development and malignancy. The role of apoptosis-related caspases in cancer remains controversial, particularly in oral tongue squamous cell carcinoma (OTSCC). In this study, we examined the protein levels of cleaved caspase-3, caspase-3, caspase-8, and caspase-9 on tissue microarrays consisting of samples from 246 OTSCC patients by immunohistochemistry. Wilcoxon signed-rank test indicated that the protein levels of cleaved caspase-3, caspase-3, caspase-8, and caspase-9 in tumor tissues were significantly higher compared to those in adjacent normal tissues (all p<0.001). The expression level of caspase-8 in tumors was elevated in patients with lymph node invasion. Moreover, positive expression of cleaved caspase-3 was associated with shorter disease-free survival (DFS) in OTSCC patients with moderate differentiation and lymph node invasion. Combination of either positive cleaved caspase-3 or higher caspase-3 expression or both was associated with poor DFS. Interestingly, stratification analysis showed that co-expression levels of positive cleaved caspase-3 or/and higher caspase-3 were associated with better disease-specific survival in patients with advanced stages of the disease, such as large tumor size and lymph node invasion, whereas it was associated with poor DFS in OTSCC patients with moderate cell differentiation and small tumor size. Taken together, cleaved caspase-3 and caspase-3/8/9 could be biomarkers for tumorigenesis in OTSCC patients. The co-expression level of cleaved caspase-3 and caspase-3 might be a prognostic biomarker for OTSCC patients, particular in those patients with certain tumor stages and cell differentiation status.</p></div
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