DataSheet1_Identification of a Glycosyltransferase Signature for Predicting Prognosis and Immune Microenvironment in Neuroblastoma.pdf

Neuroblastoma (NB) is one of the most common solid tumors in children. Glycosyltransferases (GTs) play a crucial role in tumor development and immune escape and have been used as prognostic biomarkers in various tumors. However, the biological functions and prognostic significance of GTs in NB remain poorly understood. The expression data from Gene Expression Omnibus (GEO) and Therapeutically Applicable Research to Generate Effective Treatments (TARGET) were collected as training and testing data. Based on a progression status, differentially expressed GTs were identified. We constructed a GTscore through support vector machine, least absolute shrinkage and selection operator, and Cox regression in NB, which included four prognostic GTs and was an independent prognostic risk factor for NB. Patients in the high GTscore group had an older age, MYCN amplification, advanced International Neuroblastoma Staging System stage, and high risk. Samples with high GTscores revealed high disialoganglioside (GD2) and neuron-specific enolase expression levels. In addition, a lack of immune cell infiltration was observed in the high GTscore group. This GTscore was also associated with the expression of chemokines (CCL2, CXCL9, and CXCL10) and immune checkpoint genes (cytotoxic T-lymphocyte–associated protein 4, granzyme H, and granzyme K). A low GTscore was also linked to an enhanced response to anti–PD-1 immunotherapy in melanoma patients, and one type of tumor was also derived from neuroectodermal cells such as NB. In conclusion, the constructed GTscore revealed the relationship between GT expression and the NB outcome, GD2 phenotype, and immune infiltration and provided novel clues for the prediction of prognosis and immunotherapy response in NB.</p

Additional file 4 of Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis

Additional file 4: Table S4. Primer sequences for RT-qPCR. Arid5a, AT-rich interactive domain-containing protein 5a; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; F, forward; R, reverse

Propofol Protects against Cerebral Ischemia/Reperfusion Injury by Down-Regulating Long Noncoding RNA SNHG14

Cerebral ischemia-reperfusion (CI/R) injury is a serious central nervous system disease. Propofol (PPF) exerts a neuroprotective effect in CI/R injury; the underlying cause is still unclear. Here, we cultured mouse hippocampal neuron (HT22 cells) in oxygen-glucose deprivation/reoxygenation (OGD/R) conditions to mimic CI/R injury in vitro. PPF treatment promoted cell viability and reduced apoptotic cells in the OGD/R-treated HT22 cells, which was effectively abrogated by SNHG14 overexpression. Moreover, we constructed a CI/R injury mouse model on C57BL/6J mice by middle cerebral artery occlusion/reperfusion (MCAO/R), followed by administration of PPF. PPF reduced neuronal damage and loss, enhanced glial cell hyperplasia, and ameliorated cerebral cortex tissue damage and brain infarct in MCAO/R-induced mice. SNHG14 overexpression aggravated MCAO/R-induced CI/R injury in mice. Furthermore, SNHG14 promoted the expression of Atg5 and Beclin 1 via competitively binding miR-30b-5p, which contributed to activate autophagy and apoptosis in HT22 cells. In addition, the levels of p-p38 and p-SP1 were reduced in the OGD/R-treated HT22 cells in the presence of PPF. SP1 interacted with the promoter of SNHG14 and elevated the expression of SNHG14. PPF treatment inhibited the SP1-mediated up-regulation of SNHG14. In conclusion, this work demonstrates that PPF inhibits SNHG14 expression though the p38 MAPK signaling pathway. SNHG14 promotes Atg5 and Beclin 1 expression by sponging miR-30b-5p and thus activates autophagy and aggravates CI/R injury

Additional file 2 of Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis

Additional file 2: Table S2. Detailed differential analysis results of the 32 genes obtained from the GSE121038 dataset

Additional file 1 of Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis

Additional file 1: Table S1. Sample grouping in the GSE121038 microarray datase

Additional file 6 of Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis

Additional file 6: Figure S2. Representative Western blots. A, Representative Western blots of Figure 3C. B, Representative Western blots of Figure 3I. C, Representative Western blots of Figure 4C. D, Representative Western blots of Figure 4D. E, Representative Western blots of Figure 5B. F, Representative Western blots of Figure 5I. G, Representative Western blots of Figure 5J. H, Representative Western blots of Figure 6A. I, Representative Western blots of Figure 6B. The mouse experiments were performed 14 days after AP modeling, with n = 8 for mice in each group. The cell experiment was conducted three times independently

Additional file 8 of Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis

Additional file 8: Figure S4. Rbpjl downregulates Arid5a expression and thus inhibits the IL-6/STAT3 axis to alleviate inflammatory response in control pancreatic acinar cells. A, mRNA expression of Rbpjl, Arid5a and IL-6 in control MPC-83 cells treated with oe-Rbpjl or combined with oe-Arid5a for 72 h determined by RT-qPCR. B, Rbpjl, Arid5a and STAT3 protein expression in MPC-83 cells treated with oe-Rbpjl or combined with oe-Arid5a for 72 h determined by Western blot assay. C, CCK-8 assay was used to detect control MPC-83 cell viability following treatment with oe-Rbpjl or combined with oe-Arid5a for 72 h. D, CCK-8 assay was used to detect control MPC-83 cell viability following treatment with oe-Arid5a or combined with JSI-124 for 72 h. E, Apoptosis of control MPC-83 cells following treatment with oe-Rbpjl or combined with oe-Arid5a for 72 h detected by flow cytometry. F, Apoptosis of control MPC-83 cells following treatment with oe-Arid5a or combined with JSI-124 for 72 h detected by flow cytometry. G, Ultraviolet spectrophotometers were used to detect GSH and MDA production in control MPC-83 cells following treatment with oe-Rbpjl or combined with oe-Arid5a for 72 h. H, Ultraviolet spectrophotometers were used to detect GSH and MDA production in control MPC-83 cells following treatment with oe-Arid5a or combined with JSI-124 for 72 h. I-J, TNF-α, IL-1β and IL-6 expression in control MPC-83 cells following treatment with oe-Arid5a or combined with JSI-124 for 72 h. * p < 0.05 vs. control MPC-83 cells treated with oe-NC. # p < 0.05 vs. control MPC-83 cells treated with oe-Rbpjl + oe-NC. The cell experiment was conducted three times independently

Additional file 7 of Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis

Additional file 7: Figure S3. Detection of the Rbpjl protein expression and expression of pro-inflammatory factors in pancreatic acinar cells. A, RT-qPCR and Western blot assay were used to detect the protein expression of Rbpjl after pancreatic acinar cells with oe-Rbpjl or sh-Rbpjl (for 72 h) were stimulated by LPS (for 24 h) (* p < 0.05 vs. cells treated with sh-NC. # p < 0.05 vs. cells treated with oe-NC). B, The expression of pro-inflammatory factors in the supernatant of pancreatic acinar cells with oe-Rbpjl or combined with oe-Arid5a (for 72 h) stimulated by LPS (for 24 h) was detected by ELISA. (* p < 0.05 vs. cells treated with LPS + oe-NC. # p < 0.05 vs. cells treated with LPS + oe-Rbpjl + oe-NC) C, The expression of pro-inflammatory factors in the supernatant of pancreatic acinar cells with oe-Arid5a (for 72 h) or combined with JSI-124 (for 24 h) stimulated by LPS (for 24 h) was detected by ELISA. (& p < 0.05 vs. cells treated with LPS + oe-Arid5a + DMSO) The cell experiment was conducted three times independently

Additional file 5 of Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis

Additional file 5: Figure S1. Detection of pancreatic tissue injury in mice and the expression of pro-inflammatory factors in the cell supernatant of pancreatic acinar cells. A, HE staining for the severity of pancreatic tissue injury in sham-operated or AP mice (* p < 0.05 vs. sham-operated mice). B, The weight ratio of pancreas to total body of sham-operated or AP mice (* p < 0.05 vs. sham-operated mice). C, Western blot assay detection of PAP-I protein in control or LPS-induced pancreatic acinar cells (for 24 h). * p < 0.05 vs. control cells. D, The expression of pro-inflammatory factors in the supernatant of control or LPS-induced pancreatic acinar cells (for 24 h) detected by ELISA. * p < 0.05 vs. control cells. E, The expression of pro-inflammatory factors in the supernatant of pancreatic acinar cells with oe-Rbpjl or sh-Rbpjl (for 72 h) stimulated by LPS (for 24 h) was detected by ELISA. * p < 0.05 vs. cells treated with LPS + oe-NC. # p < 0.05 vs. cells treated with LPS + sh-NC. The mouse experiments were performed 14 days after AP modeling, with n = 8 for mice in each group. The cell experiment was conducted three times independently