Bradfordkromann2700

Results The results revealed that high expression of NFE2L3 was positively associated with malignant behavior and EMT in HCC. Knockdown of NFE2L3 inhibited cell proliferation and migration, led to cell cycle G0/G1 arrest and induction of cell apoptosis, increased expression of E-cadherin and decreased expression of N‑cadherin, Vimentin, MMP2, CDK2 and PCNA. In addition, tumor growth was inhibited by silencing of NFE2L3 in vivo. Expression of β-catenin and Wnt target genes cyclin D1 and TCF4 was reduced in HepG2-shNFE2L3 cells. Conclusions NFE2L3 promotes cell proliferation, metastasis, and induces EMT of hepatocellular carcinoma (HepG2) cells via activation of Wnt/β-catenin pathway.Background Metabolomics has demonstrated its potential in the early diagnosis, drug safety evaluation and personalized toxicology research of various cancers. Objectives We aim to screen for potential diagnostic and capecitabine-related adverse effect (CRAE) biomarkers from urinary endogenous metabolites in Chinese colorectal cancer (CRC) patients. Methods The metabolic profiles of 139 CRC patients and 50 non-neoplastic controls were analyzed using ultra-high-performance liquid chromatography combined with quadrupole time-of-flight mass spectrometry. Results There were 41 metabolites identified between the CRC patients and the non-neoplastic controls, and 19 metabolites were identified between CRC patients with and without CRAE. Based on these identified metabolites, bioinformatic analysis and prediction model construction were completed. Most of these differential metabolites have important roles in cell proliferation and differentiation and the immune system. Based on binary logistic regression, a CRC prediction model, composed of 3-methylhistidine, N-heptanoylglycine, N1,N12-diacetylspermine and hippurate, was established, with an area under curve (AUC) of 0.980 (95% CI 0.953-1.000; sensitivity 94.3%; specificity 92.0%) in the training set, and an AUC of 0.968 (95% CI 0.933-1.000; sensitivity 89.9%; specificity 92.0%) in the testing set. In addition, methionine and 4-pyridoxic acid can be combined to predict hand foot syndrome, with an AUC of 0.884; ubiquinone-1 and 4-pyridoxic acid can be combined to predict anemia, with an AUC of 0.889; and 5-acetamidovalerate and 3,4-methylenesebacic acid can be combined to predict neutropenia, with an AUC of 0.882. Conclusion The profiling of urine polar metabolites has great potential in the early detection of CRC and the prediction of CRAE.Purpose To evaluate the association of clinical early response and pathological complete remission (pCR) in breast cancer patients with different molecular subtypes. Materials and methods Breast cancer patients who received neoadjuvant treatment (NAT) with clinical early response assessment from October 2008 to October 2018 were retrospectively analyzed. Clinical early response was defined as tumor size decreasing ≥30% evaluated by ultrasound after two cycles of NAT. Chi-square test was used to compare the pCR rates between the responder and non-responder groups with different molecular subtypes. Multivariate logistic regression was used to identify independent factors associated with the pCR. Results A total of 328 patients were included 100 responders and 228 non-responders. The progesterone receptor (PR) expression was an independent factor associated with clinical early response (OR=2.39, 95%CI=1.41-4.05, P=0.001). The pCR rate of breast was 50.0% for responders and 18.0% for non-responders (P less then 0.001). Regarding different molecular subtypes, responders had higher pCR rates than non-responders for patients with HER2 overexpression (OR=10.66, 95%CI=2.18-52.15, P=0.001), triple negative (OR=3.29, 95%CI=1.23-8.84, P=0.016) and Luminal (HER2-) subtypes (OR=8.58, 95%CI=3.05-24.10, P less then 0.001) respectively. Moreover, pCR rate can be achieved as high as 88.2% in HER2 overexpression patients with early clinical response, which was significantly higher than patients without early response (41.3%, P=0.001). Multivariate analysis showed that clinical early response was an independent factor associated with the pCR rate (OR=4.87, 95%CI=2.72-8.72, P less then 0.001). Conclusions Early response was significantly associated with a higher pCR rate in breast cancer patients receiving NAT, especially for patients with HER2 overexpression subtype, which warrants further clinical evaluation.Traditional anticancer therapies can cause serious side effects in clinical treatment due to their nonspecific of tumor cells. Aptamers, also termed as 'chemical antibodies', are short DNA or RNA oligonucleotides selected from the synthetic large random single-strand oligonucleotide library by systematic evolution of ligands by exponential enrichment (SELEX) to bind to lots of different targets, such as proteins or nucleic acid structures. Aptamers have good affinities and high specificity with target molecules, thus may be able to act as drugs themselves to directly inhibit the proliferation of tumor cells, or own great potentialities in the targeted drug delivery systems which can be used in tumor diagnosis and target specific tumor cells, thereby minimizing the toxicity to normal cells. Here we review the unique properties of aptamer represents a great opportunity when applied to the rapidly developing fields of biotechnology and discuss the recent developments in the use of aptamers as powerful tools for analytic, diagnostic and therapeutic applications for cancer.Transforming growth factor β1 (TGF-β1) plays an important role in tumor initiation and development by inducing epithelial-mesenchymal Transition (EMT). Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long noncoding RNA (lncRNA) that contributes to the invasion and metastasis of tumors, including esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the underlying mechanisms implicated in EMT and to clarify whether TGF-β1 regulates MALAT1 expression, thereby promoting the invasion of ESCC. Expression of TGF-β1, MALAT1 and EMT-related markers, including E-cadherin and Vimentin, was detected in clinical samples of Kazakh's ESCC. The role of TGF-β1 in the regulation of MALAT1 in ESCC invasion was evaluated at the ESCC cell line level. read more High TGF-β1 expression was significantly associated with poor survival among patients with Kazakh's ESCC. Additionally, the expression of Vimentin was upregulated, and the expression of E-cadherin was downregulated and varied. The expression of MALAT1 positively correlated with the expression of TGF-β1 both in vivo and in vitro.