Temozolomide (TMZ) is a commonly used anti-glioblastoma (GBM) drug. However, glioblastoma cells frequently show primary and acquired resistance to TMZ. As a promising anti-GBM candidate, resveratrol (Res) faces the similar problem as TMZ. Although resveratrol combined with TMZ (Res/TMZ) has been reported to be used to treat GBMs, it remains unclear whether this combination is broad-spectrum for all glioma cells until now, especially for GBM cells/cases with dual drug resistance. The study aimed to evaluate the synergistic effects of resveratrol and TMZ against GBMs and identify the underlying mechanisms. Drug sensitivities of rat RG-2, human LN-18 and LN-428 cell lines and effectiveness of Res/TMZ combinations were investigated via multiple experimental methods. O -methylguanine-DNA methyltransferase (MGMT) was observed by Western blotting and immunocytochemistry (ICC). Transducer and activator of transcription 3 (STAT3) signaling pathway and expression changes of -related gene were detected to exploreerapy. Our results demonstrated synergistic effects of Res/TMZ on RG-2 cells and their bilaterally sensitizing effects to LN-18 and LN-428 cells. Frequent upregulation of MGMT and activation of STAT3 are the unfavorable factors for the treatment of GBMs and they may be the potential targets of Res/TMZ therapy. Aim of this study was to identify biomarkers between different grades of bladder cancer (BLCA) and its prognostic value. mRNA expression data from GSE32549 and GSE71576 were extracted for further analysis. Differentially expressed genes (DEGs) were identified using GEO2R web tool. Gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and protein-protein interaction (PPI) network were conducted to explore the function and relationship of DEGs. The Cancer Genome Atlas (TCGA) database was used for external validation and Gene set enrichment analysis (GSEA) analysis was used to further identify FADS1 pathways. Bladder cancer cells and patient specimens were used to further demonstrate the function of FADS1. Datasets from GEO identified a panel of DEGs. Functional enrichment analysis highlighted that DEGs were associated with nuclear division, spindle, cell cycle and p53 signaling pathway. External validation from TCGA demonstrated that FADS1 was an independent prognostic marker in BLCA patients. In cell lines and tumor specimen analysis, FADS1 was overexpressed in the tumor specimen, compared with adjacent tissues, and positively correlated with tumor grade of BLCA. Moreover, FADS1 could enhance the proliferation ability and influence cell cycle of bladder cancer cells. FADS1 was an independent prognostic biomarker for BLCA and could confer the bladder cancer cells increased proliferation ability. FADS1 was an independent prognostic biomarker for BLCA and could confer the bladder cancer cells increased proliferation ability. Pathological complete response (pCR) is the goal of neoadjuvant chemotherapy (NAC) for the HER2-positive and triple-negative subtypes of breast cancer and is related to survival benefit; however, luminal breast cancer is not sensitive to NAC, and the size of tumor shrinkage is a more meaningful clinical indicator for the luminal breast cancer subtype. We wanted to use a nomogram or formula to develop and implement a series of prediction models for pCR or tumor shrinkage size. We developed a prediction model in a primary cohort consisting of 498 patients with invasive breast cancer, and the data were gathered from July 2016 to September 2018. The endpoint was pCR and tumor shrinkage size. In the primary cohort, the HER2-positive cohort, and the triple-negative cohort, multivariate logistic regression analysis was used to screen the significant clinical features and clinicopathological features to develop nomograms. In the luminal group, multivariate linear regression analysis was used to test the risk facttify patients at high probability for pCR after NAC. Clinicians can stratify these patients and make individualized and personalized recommendations for therapy. Utilizing this predictive model will enable us to identify patients at high probability for pCR after NAC. Clinicians can stratify these patients and make individualized and personalized recommendations for therapy. Non-small cell lung cancer (NSCLC) is a typical epithelial lung cancer with high metastasis, incidence and mortality. In recent years, long noncoding RNA small nucleolar RNA host gene 7 ( ) has been identified as significant regulator in different cancer types, including NSCLC. However, the underlying molecular mechanism of during NSCLC tumorigenesis and progression remains largely unclear. and miR-181a-5p expression in NSCLC tumors and cells were detected by qRT-PCR. Cell viability, migration, invasion and apoptosis were evaluated by CCK-8, transwell and flow cytometry assay, respectively. A549 and NCI-H1299 xenograft mice model was constructed by subcutaneously injecting cells stably transfected with sh-SNHG7 and sh-NC. The interaction between and miR-181a-5p was validated by luciferase reporter system, RIP and RNA pull down assay. Protein expression of cleaved caspase 3, proliferating cell nuclear antigen (PCNA), AKT, p-AKT, mammalian target of rapamycin (mTOR) and p-mTOR was analyzed by Western blot. expression was up-regulated while miR-181a-5p expression was down-regulated in NSCLC tumors, especially those from patients at Phase III+IV, compared with normal tissues. However, depletion attenuated tumor growth in vitro and in vivo. https://www.selleckchem.com/products/sch772984.html Moreover, miR-181a-5p inhibitor abolished silencing induced inhibition on proliferation, migration and invasion in NSCLC. Subsequently, we found modulated cell progression by targeting miR-181a-5p and activating AKT/mTOR signaling pathway. SNHG7 accelerates proliferation, migration and invasion of NSCLC by suppressing miR-181a-5p through AKT/mTOR signaling pathway, thus presenting desirable biomarkers for NSCLC therapy. SNHG7 accelerates proliferation, migration and invasion of NSCLC by suppressing miR-181a-5p through AKT/mTOR signaling pathway, thus presenting desirable biomarkers for NSCLC therapy.