Salisburyburnett8872
A number of studies have found that metabolic disorders are the characteristic manifestations of tumor cells. However, the effects of hypoxic environment on mitochondrial function and glucose metabolism of tumor cells were still unclear. The study wanted to explore the regulatory mechanism of hypoxic environment on mitochondrial function and metabolism in gastric cancer cells.
The animal model of gastric cancer and MKN45 were treated in a hypoxic environment. Mitochondrial membrane potential and reactive oxygen species (ROS) levels were analyzed by flow cytometry, qPCR was used to detect the expression levels of glycose metabolism key enzymes, damage repair genes and mitochondrial DNA (mtDNA) copy numbers in gastric cancer.
Compared with 2,000 m normal gastric cancer tissue, the decreased of mitochondrial membrane potential and the production of ROS reduced, the expressions of glucose metabolism genes [the M1 isoform of Hexokinase (HK1), pyruvate kinase (PKM), Succinate dehydrogenase (SDHA), Glucose-6-phosphate dehydrogenase (G6PD)], homologous recombination repair gene (RAD51) and repair DNA double-stranded broken gene (ASTCT2) increased, and aerobic respiration reduced in gastric cancer cells. In the hypoxic environment, the decreased of mitochondrial membrane potential reduced, the production of ROS and mtDNA copies increased, HK1 expression increased, the expressions of SDHA, G6PD, RAD51 and ASCT-2 decreased, and the aerobic respiration decreased.
Hypoxia plays an important role in maintaining mitochondrial functions in gastric cancer cells by promoting glycolysis and inhibiting mitochondrial aerobic respiration capacity.
Hypoxia plays an important role in maintaining mitochondrial functions in gastric cancer cells by promoting glycolysis and inhibiting mitochondrial aerobic respiration capacity.
The aim of the present study was to identify key genes and pathways downstream of S100PPBP in pancreatic cancer cells.
The microarray datasets GSE35196 (S100PBP knockdown) and GSE35198 (S100PBP overexpression) were downloaded from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were obtained separately from GEO2R, and heatmaps showing clustering analysis of DEGs were generated using R software. Gene Ontology and pathway enrichment analyses were performed for identified DEGs using the Database for Annotation, Visualization, and Integrated Discovery and Kyoto Encyclopedia of Genes and Genomes, respectively. A protein-protein interaction (PPI) network was created using the Search Tool for the Retrieval of Interacting Genes and Cytoscape software. Relevant expression datasets of key identified genes were downloaded from The Cancer Genome Atlas, and overall survival (OS) analysis was performed with R software. Finally, Gene Expression Profiling Interactive Analysis was used to evaluateancer cell adhesion.
Rab25, a hub node of protein-protein interaction networks, has become one of the most popular tumor-associated proteins. Pyruvate kinase (PK) is the main rate-limiting enzyme in the glycolysis pathway and plays a significant role in the regulation of Warburg effect. In this study, we aimed to characterize the expression and function of Rab25 in gastric adenocarcinoma (GAC) and verify our hypothesis experimentally that Rab25 may participate in the regulation of aerobic glycolysis via PKM2 (a subtype of PK) in GAC.
The impact of Rab25 expression on patient overall survival was estimated using the Kaplan-Meier method. Rab25 expression was silenced or increased respectively by lentivirus-mediated transfection. To assess the role of Rab25 in cell viability
, cell proliferation and migration experiments were performed. Levels of pyruvate and lactic acid were detected by kits. Immunofluorescence analysis and Co-Immunoprecipitation were performed to explore the interaction between Rab25 and PKM2 protein.
High Rab25 expression was associated with reduced patient overall survival. Panobinostat Silencing Rab25 inhibits GAC cells proliferation and overexpressing Rab25 promotes cell proliferation and migration in gastric cells
. The study revealed that Rab25 participates in the positive regulation of aerobic glycolysis in GAC cells. Rab25 protein and PKM2 protein co-located on the cell membrane and could bind to each other in GAC cells. Rab25 is a positive regulator of PKM2 and Rab25 up-regulation promotes phosphorylation of PKM2.
In human GAC, Rab25 predicts poor prognosis and regulates aerobic glycolysis via phosphorylating PKM2-Y105.
In human GAC, Rab25 predicts poor prognosis and regulates aerobic glycolysis via phosphorylating PKM2-Y105.
Programmed cell death protein 1 (PD-1) blockade is a major advance in the treatment of malignancies, but there remain many problems in efficacy evaluation. The aim of this study was to determine whether dynamic monitoring of serum specific tumor markers (SSTMs) could predict the response to PD-1 blockade and prognosis in patients with malignancies.
The dynamic changes in SSTMs in 27 patients between January 1, 2018 and July 31, 2019 were analyzed retrospectively. The association between the SSTM response and the radiological response was evaluated using the χ
test and Spearman's correlation analysis. Kaplan-Meier estimates and the log rank test were used to explore the correlation of SSTM dynamics with progression-free survival (PFS) and overall survival (OS).
In this study, 85.3% of patients with malignant tumors had detectable SSTM. According to the changes of SSTM within the first 12 weeks of treatment, the patients were divided into a tumor marker increased group and a tumor marker decreased groupict the prognosis of patients with malignancies; it may also be helpful for clinical judgment of pseudoprogression and delayed response.
Dynamic monitoring of SSTMs can be used as a necessary supplement to imaging examination to evaluate the response to PD-1 blockade and predict the prognosis of patients with malignancies; it may also be helpful for clinical judgment of pseudoprogression and delayed response.
Chromodomain helicase DNA binding protein 5 (CHD5) was reported to be a tumor suppressor and our previous work showed CHD5 was epigenetically inactivated in human chronic myeloid leukemia (CML). This study aimed to investigate the effect of its overexpression on CML tumorigenesis.
Quantitative reverse-transcriptase PCR and Western blotting analysis were used to detect the expression of CHD5 in human CML cell lines. The endogenous CHD5 expression was activated in two CML cell lines by CRISPR/dCas9-SAM system.
cell function experiments were performed including proliferation, colony formation, apoptosis, autophagy, senescence and differentiation assays. Furthermore, tumorigenicity was evaluated
in nude mice xenograft model.
CHD5 was down-regulated in CML cell lines compare to normal bone marrow mononuclear cells (MCs). Cell proliferation after activating CHD5 was significantly inhibited. Moreover, overexpression of CHD5 induced G2/M phase arrest and apoptosis in CML cells. In a tumor xenograft mouse model, CHD5 restoration was found to sharply repress tumor growth. Compared with the control group, overexpression of CHD5 enhanced the expression of p21 and cdc2 phosphorylation, whereas decreased the protein level of Cyclin B1. Furthermore, experiments revealed that up-regulation of CHD5 activated caspase-3, while anti-apoptosis protein Bcl-2 expression was reduced in CML cells.
CHD5 plays a role of anti-tumorigenic effects involved in CML cell proliferation, cell cycle arrest and apoptosis.
CHD5 plays a role of anti-tumorigenic effects involved in CML cell proliferation, cell cycle arrest and apoptosis.
Colloid adenocarcinoma of the lung is one of rare subtypes of pulmonary adenocarcinoma. The purpose of our study is to establish a predictive model for the overall survival of colloid adenocarcinoma.
A total of 749 patients were separated from the Surveillance, Epidemiology, and End Results database between 2011 and 2015. Cox regression was performed to select the predictors of overall survival. The calibration curves, concordance index, the receiver operating characteristic curve, and the area under the curve were used to verify the nomogram. Kaplan-Meier curves were used to illustrate and compare the overall survival of patients in different surgical groups.
Multivariate analyses demonstrated clinical characteristics such as age, sex, race, site, tumor stage, stage T, metastatic sites at diagnosis, surgical treatment were associated with prognosis. In the nomogram, we could predict the probability of overall survival for patients. The concordance index of the novel nomogram was 0.849, which meant that and give treatment recommendations.
The aim was to explore the interaction among chemokine (C-X-C motif) ligand (CXCL) 1/2/8 expressions, and their associations with clinicopathologic features and survival profiles in non-small cell lung cancer (NSCLC) patients.
The tumor tissue specimens from 232 primary NSCLC patients with TNM stage I-IIIA underwent resection were obtained and the expressions of CXCL1, CXCL2 and CXCL8 were measured by immunohistochemical assay. Disease-free survival (DFS) and overall survival (OS) were calculated according to survival data.
There were 117(50.4%) CXCL1 low expression patients versus (
.) 115 (49.6%) CXCL1 high expression patients, 107(46.1%) CXCL2 low expression patients
. 125 (53.9%) CXCL2 high expression patients, 93 (40.1%) CXCL8 low expression patients
. 139 (59.9%) CXCL8 high expression patients. Meanwhile, CXCL1 expression was positively correlated with CXCL2 expression and CXCL8 expression; CXCL2 expression was also positively correlated with CXCL8 expression. For tumor features, CXCL1, CXCL2 and CXCL8 were positively correlated with lymph node (LYN) metastasis and TNM stage, but not correlated with differentiation, tumor size or carcinoembryonic antigen (CEA) level. For prognosis, CXCL1 high expression was associated with worse DFS and OS, so did CXCL2 high expression, while there was no correlation of CXCL8 with DFS or OS; Multivariate Cox's regression disclosed that high expression of CXCL1, but not CXCL2 or CXCL8, was an independent factor predicting shorter DFS and OS.
An inter-correlation is observed among CXCL1, CXCL2 and CXCL8 expressions, and they show diversified potential as biomarkers for tumor features and survival profiles in NSCLC patients.
An inter-correlation is observed among CXCL1, CXCL2 and CXCL8 expressions, and they show diversified potential as biomarkers for tumor features and survival profiles in NSCLC patients.
Retinoblastoma (RB), depicted as an aggressive eye cancer, mainly occurs in infancy and childhood and is followed by high mortality and poor prognosis. Increasing evidence has revealed that long noncoding RNA taurine upregulated gene 1 (TUG1) is closely linked to the progression of diverse cancers. Nonetheless, the specific function and molecular regulatory mechanism of TUG1 in RB still need to be explored.
To explore the specific role of TUG1 in RB. TUG1 expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell counting kit-8 (CCK-8), colony formation, 5-ethynyl-2'-deoxyuridine (EdU), caspase-3, terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) and western blot assays were utilized to study the role of TUG1 in RB. The binding relation between miR-516b-5p and TUG1 or hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase (H6PD) was analyzed by luciferase reporter and RNA immunoprecipitation (RIP) assays.
The expression of TUG1 was upregulated in RB cells.
