Dalyforrest4713

The lower expression level of miR-195 was positively correlated with advanced clinical stage. In addition, we showed that the expression of miR-195 was negatively correlated with the LINC00473 expression level in colorectal cancer tissues. LINC00473 accelerated colorectal cancer cell proliferation and cell cycle progression and regulated EMT progression by regulating miR-195 expression. These data suggested that LINC00473 induced cell proliferation, cell cycle progression and EMT progression by acting as a ceRNA for miR-195 in colorectal cancer.EGFR/EGFR variant III (EGFRvIII) glioblastoma is seriously malignant, and the underlying mechanism remains unclear. In this study, EGFR and GLUT3 were found to be co-expressed in our collected tissues and associated with worse overall survival in glioblastoma via bioinformatics analysis. Functionally, in vitro and in vivo tests revealed that silencing GLUT3 substantially inhibited the viability of U87-EGFRvIII and LN229-EGFRvIII cells. Compared with wild-type U87 or LN229 cells, the expression level of SOX9 in U87-EGFRvIII or LN229-EGFRvIII cells (U87 and LN229 over-expressing EGFRvIII) was substantially increased. Chromatin immunoprecipitation and Dual-luciferase reporter assays revealed that SOX9 bound to the promoter of GLUT3 and promoted the expression of GLUT3. Collectively, our findings indicated that the EGFR/EGFRvIII-SOX9-GLUT3 axis mediated the tumourigenesis of glioblastoma and might be a potential target for glioblastoma therapy.

To analyze the role of circMYC in cervical cancer.

Protein and RNA expression was detected by RT-qPCR and western blotting. Selleckchem Navitoclax Transwell, CCK8, and colony formation assays were used for measuring metastasis, cell viability, and proliferation, respectively. Lactate production, glucose uptake, and ATP generation were examined to evaluate cell glycolysis. Interactions between circMYC, miR-577, and MET were determined by RNA pull-down and immunoprecipitation, and dual-luciferase reporter assays. Xenografts were established in mice to evaluate the functions of circMYC

.

circMYC was overexpressed in tumor tissue, which was related to poor prognosis. CircMYC knockdown reduced proliferation, colony formation, metastasis, and glycolysis in cervical cancer cells as well as inhibiting tumor growth

. Mechanistically, circMYC targeted miR-577, and the effects of circMYC knockdown could be reversed by miR-577 inhibition. Moreover, miR-577 downregulated the expression of MET. Therefore, the oncogenic role of circMYC in cervical cancer was achieved by sponging miR-577 and maintaining MET expression.

circMYC promotes cervical cancer progression through regulation of the miR-577/MET axis. circMYC may thus be a potential target for diagnosing and treating cervical cancer.

circMYC promotes cervical cancer progression through regulation of the miR-577/MET axis. circMYC may thus be a potential target for diagnosing and treating cervical cancer.Acetaminophen (APAP) overdose has been considered responsible for the drug-induced liver injury for many years. Ferroptosis is defined as an iron-dependent form of cell death associated with lipid peroxide accumulation. Ferroptosis is involved in APAP-induced acute liver failure, and UTI is an effective drug treatment for acute liver failure. Thus, we aimed to determine whether UTI protects the liver against APAP-induced acute liver failure by decreasing ferroptosis-induced lipid peroxide accumulation. C57BL/6 mice and LO2 cell line were treated with UTI before and after the exposure to APAP. Liver tissues and LO2 cells were collected for biochemical assessment of molecular parameters. APAP-induced upregulation of ferroptotic events (iron content), lipid hydroperoxides (ROS production, MDA, and 4-HNE), and depletion of GSH were effectively relieved by ferrostatin-1 (Fer-1), a ferroptosis inhibitor, and UTI. UTI blocked ferroptosis-induced lipid peroxide accumulation by promoting nuclear translocation of NRF2 to activate its downstream targets (HO-1). An increased expression or knockdown of of SIRT1 influenced the UTI effect on the NRF2 pathway and had an impact on lipid accumulation. Overall, UTI plays a role in mitigation of APAP-induced acute liver injury by inhibiting ferroptosis-induced lipid peroxide accumulation, and the effect of UT1 was mediated by the NRF2/HO-1 pathway and SIRT1 expression.

This study investigated the effects and mechanism of high-fat diet on the epithelial-mesenchymal transition (EMT) of respiratory tract and the intervention of saturated hydrogen on it.

80 five-week-old C57BL6/J male mice were randomly divided into normal control group, H

group, high-fat (HF) group and HF+H

group, making 20 mice in each group. The weights of the mice were measured on weekly basis. Six mice from each group were executed at every second week. Blood samples were collected for lipid testing. Lung tissues were collected for 16S rRNA gene sequencing, HE staining, immunofluorescence and quantitative real-time PCR (qPCR).

Compared with the control group, the mice in the HF group showed increased inflammatory cell infiltration, decreased expression of e-cadherin (E-cad) and increased expression of Twist. There were significant differences in the composition of bacteria in the lung, and the expression of isocitrate lyase (ICL) genes in

and

, which were significantly associated with asthma were seen with a significant increasing trend. After the treatment of saturated hydrogen, the changes in lung microbial population, lung tissue infiltration of inflammatory cells and the transformation of epithelial stroma caused by high-fat diet were moderately alleviated.

High-fat diet can promote inflammation and EMT in the lung by enlarging the growth of glyoxylic acid cycle-dependent bacteria, and the pathological process are partly alleviated by saturated hydrogen.

High-fat diet can promote inflammation and EMT in the lung by enlarging the growth of glyoxylic acid cycle-dependent bacteria, and the pathological process are partly alleviated by saturated hydrogen.Circular RNAs (circRNAs) in exosomes exhibit stable expression and are not easily degraded in plasma; a characteristic that makes them ideal as novel non-invasive tumor diagnostic markers. In this study, we examined different expression of circRNA in plasma exosomes of primary hepatocellular carcinoma patient and healthy volunteer by full transcriptome sequencing. Five circRNAs with up-regulated expression were selected, and large sample size verified their expression. Among them, it is further confirmed that exo_circ_0006602 is up-regulated in the large sample cohort. In addition, the expression level of exo_circ_0006602 was correlated with HBsAg (P less then 0.011), HBeAg (P=0.048), liver cirrhosis (P=0.001) and Edmondson-Steiner grade (P less then 0.001). The receiver operating characteristic (ROC) was used to evaluate the accuracy of exo_circ_0006602 as a diagnostic marker. The AUC value of exo_circ_0006602 was significantly highter than common serum tumor markers AFP and CEA. Exo_circ_0006602 combined with AFP can significantly improve the diagnostic accuracy. Cell function experiments show that exo_circ_0006602 can significantly improve the proliferation and invasion ability of liver cancer cell lines and also promoted the expression of tumor proliferation-related protein Snail. In conclusion, our results suggested that exo_circ_0006602 can be used as a potential non-invasive biomarker for the early diagnosis and screening of liver cancer, the sensitivity and specificity of diagnosis are higher than traditional tumor markers.In vitro cell experiments showed that knocking out the placenta-specific protein 8 (PLAC8) gene significantly increased the sensitivity of tumor cells to radiation. This study used two nude mouse models of nasopharyngeal carcinoma (NPC) to investigate the radio-sensitization and molecular mechanism of PLAC8 knockout in vivo. The expression of PLAC8 in 120 NPC tissues and 30 nasopharyngitis (NPG) tissues was detected by immunohistochemistry (IHC) to analyze the relationship between PLAC8 and neck lymph node metastasis and prognosis in NPC patients. The mRNA expression level of PLAC8 in several NPC cell lines was detected by semi-quantitative RT-PCR. The PLAC8 gene was knocked out in CNE-2 cells using CRISPR/Cas9. The effect of PLAC8 gene knockout on the radiotherapy sensitivity of NPC cells was analyzed by establishing model 1 and model 2 tumor-bearing nude mouse models with two different irradiation methods. The expression of γH2AX, Bax, Bcl-2, Caspase-3 and cleaved Caspase-3 was detected by immunofluorescencC8 expression is closely related to neck metastasis and the prognosis of NPC. PLAC8 gene knockout significantly increases the radio-sensitivity of NPC cells in vivo by promoting apoptosis, which is an effective strategy for the radiotherapy sensitization of NPC.

As a type of breast cancer that has relatively strong invasiveness, triple negative breast cancer (TNBC) seriously affects the survival of patients. microRNAs (miRNAs) have been shown to exert a prominent regulatory effect on the disease, among which miR-133b is reported to be involved in the pathological mechanism of breast cancer, but its role in TNBC remains unclear.

In this study, real-time quantitative PCR (RT-qPCR) and Western blotting (WB) were performed for detecting the expressions of miR-133b, fibroblast growth factor receptor 1 (FGFR1), and Wingless/Integrated (Wnt)-β-catenin pathway markers (Wnt1, β-catenin, nuclear-β-catenin, p-GSK-3β, GSK-3β, cyclinD1, and FOXQ1). With TNBC cells and DDP-resistant TNBC cells (TNBC/DDP cells) used as research objects, their proliferation and apoptosis were measured by Cell Counting Kit-8 (CCK-8) assays and Flow cytometry, respectively. Then, the targeted relationship between miR-133b and FGFR1 was verified by Dual luciferase reporter gene assay (DLRGA).

In our study, miR-133b was down-regulated while FGFR1 up-regulated in TNBC. The ectopic expression of miR-133b remarkably inhibited the proliferation and colony formation but induced apoptosis of TNBC cells, and inactivated the Wnt-β-catenin pathway. The knockdown of FGFR1 had similar effects. Additionally, miR-133b targeted and negatively regulated FGFR1. Up-regulating miR-133b or down-regulating FGFR1 could enhance the proliferation and DDP sensitivity of TNBC cells or TNBC/DDP cells. Up-regulating FGFR1 could offset the anti-TNBC cell survival and DDP sensitization shown by ectopic expression of miR-133b.

To sum up, miR-133b can inhibit the growth and DDP resistance of TNBC cells by targeting FGFR1 and inactivating the Wnt-β-catenin pathway.

To sum up, miR-133b can inhibit the growth and DDP resistance of TNBC cells by targeting FGFR1 and inactivating the Wnt-β-catenin pathway.Urethral stricture is one of the common diseases in urology. It can lead to obstructive voiding dysfunction and may cause long-term damage to the entire urinary tract. Here, we investigated the effect of combined use of 5-fluorouracil (5-FU) and triamcinolone acetonide (TA) in improving urethral stricture. We established urethral stricture in vivo and in vitro model. The role of TA combined with 5-FU treatment in scar tissue and fibroblast cells were examined by RT-PCR, Western blot and immunohistochemical methods. The function of miRNA in improving urethral stricture by TA combined with 5-FU treatment were further investigated. We found that TA combined with 5-FU treatment obviously prevent urethral fibrosis in vivo as well as in vitro. MiR-192-5p level was downregulated in urethral stricture tissue and urethral tissue fibroblast, TA combined with 5-FU treatment rescue the expression of miR-192-5p. The improvement of urethral fibrosis by TA combined with 5-FU treatment was blocked by miR-192-5p inhibitor. miR-192-5p mediated the improvement of urethral scar by triamcinolone acetonide combined with 5-FU by directly targeting ATG7, which is marker gene of autophagy.