74 results about "Epithelial–mesenchymal transition" patented technology

The present invention discloses a method for discriminating between sensitive and resistant tumours to a treatment with EGFR inhibitor drugs comprising: in vitro testing whether tumour material expresses the hMena^+11a splicing variant of hMe-na, the tumour positive to said testing being sensitive to the treatment.

The methods described herein allow for the classification of patients into groups for receiving optimized radiation treatment based on patient specific biomarker signature. The biomarker signature includes markers that have been shown to correlate with TGF-β expression and to be associated with tumor aggressiveness, radioresistance and poor prognosis. The markers play a key role in the epithelial-mesenchymal transition. The methods described herein provide the dual benefits of anti-tumor efficacy plus normal tissue protection when combining TGF-β inhibitors with ionizing radiation to treat cancer patients.

The invention provides application of amlexanox to inhibition of epithelial-mesenchymal transition (EMT) and anti-tumor metastasis. The effective concentration of the amlexanox for inhibition of epithelial-mesenchymal transition and anti-tumor metastasis is 100 nM to 10 muM. Whether various micromolecular compounds are EMT target points or not is screened by an efficient and dynamic screening method, the obtained amlexanox can effectively inhibit epithelial-mesenchymal transition and tumor metastasis, a new method is provided for treatment target points for treating tumor metastasis clinically, and great social and economic benefits can be brought.

The present invention relates to methods and assays for identifying agents useful in the treatment of diseases associated with epithelial mesenchymal transition (EMT), in particular fibrotic diseases and cancer. The invention provides polypeptide and nucleic acid TARGETs, siRNA sequences based on these TARGETs and antibodies against the TARGETs. The invention is further related to pharmaceutical composition comprising siRNA sequences based on the TARGETs and antibodies against the TARGETs for use in the treatment of diseases associated with epithelial mesenchymal transition, in particular fibrotic disease and cancer. The invention further provides in vitro methods for inhibition of epithelial mesenchymal transition.

The invention relates to the field of new application of drugs, specifically to application of glucosamine in preparation of a drug for preventing and treating ionizing radiation induced pulmonary injury. The structure formula of glucosamine is shown in the description. The glucosamine is used as the drug for preventing and treating ionizing radiation induced pulmonary injury, and is small in toxic and side effects, and obvious in treatment effect; the glucosamine is applied based on the concentration of 100mg/kg/d in first three days of radiation; the pulmonary tissue can be obviously protected and is inhibited from epithelial-mesenchymal transition, which is the unique feature of the glucosamine in preventing and treating of ionizing radiation induced pulmonary injury; the glucosamine has a good application prospect in the Chinese medical field.

The invention discloses a tree peony bark extract and application thereof to preparation of medicines for treating pulmonary fibrosis. At first, tree peony bark is extracted, and after that, pH value adjustment and heating for enzymolysis are carried out; after enzymolysis, the distillate is collected by the steam distillation method, left to stand and filtered to obtain crystal paeonol; the residual extracting solution and the leaves are filtered, and the herb residues are left for later use; the filtrate is subjected to concentration under reduced pressure and deproteinization, then ethanol is added, the mixture is left to stand, the ethanol solution is separated and collected for later use, and the sediment is washed to obtain cortex moutan polysaccharide; the stand-by ethanol solution is added into the stand-by herb residues for soaking and filtering, and the filtrate is subjected to concentration under reduced pressure and purification to obtain total glucosides of cortex moutan; the paeonol, the polysaccharide and the total glucosides are mixed to obtain the tree peony bark extract. Experimental results show that the tree peony bark extract can effectively inhibit epithelial-mesenchymal transition and lung fibroblast activation of alveolar epithelial cells so as to prevent pulmonary fibrosis from formation and development, and can be applied to preparation of medicines for treating pulmonary fibrosis.

The invention relates to a method for detecting the influence of a triple negative breast cancer cell on an endothelial cell secretion function in the epithelial-mesenchymal transition process. A triple negative breast cancer cell line MDA-MB-231 and a human umbilical vein endothelial cell HUVEC are selected, and experimental groups including an MDA-MB-231 and HUVEC co-culture group and a control group, namely a MDA-MB-231 individual culture group are set; after the experimental groups and the control group are applied to 10ng/ml TGF-beta stimulation for 36 hours, a TMT quantitative proteome expression profile is applied to analyze differential expressions of secretory proteins in cellular supernatants in the two groups, and secretion results of SERPINE (PAI-1) factors in the co-culture group and the individual culture group are compared. The triple negative breast cancer cell line of the triple negative breast cancer cell in the epithelial-mesenchymal transition process can promote secretion of chemotactic factors CCL5 of endothelial cells and accordingly promotes transfer of the triple negative breast cancer cell.

The invention researches biological properties of apigenin based on experiment means, and innovatively found that the apigenin has a definite inhibiting effect for liver cancer epithelial-mesenchymal transition (EMT) and can invert EMT development processes. Molecular marking experiments show that the expression level of epithelial marker molecules in apigenin-interfered liver cancer cells increases, the expression amount of mesenchymal marker molecules decreases, and degrees of changes and apigenin are in a dose-dependent manner. Based on the abovementioned beneficial findings, the apigenin can be utilized to treat a plurality of diseases adopting the EMT as an effect. The inventor further found that a relieving effect of the apigenin on the EMT effect can be adopted as a treating path for liver cancer. Experiments prove that as the liver cancer cell EMT effect is effectively inverted, metastasis of liver cancer cells is significantly inhibited and liver cancer cell proliferation is limited, thus successfully proving the cancer treating function of the apigenin.

The present invention relates to a method for scanning a cancer metastasis inhibitor by analyzing the activity of lysyl-tRNA synthetase (KRS) in a cancer cell line cultured in a three-dimensional collagen gel environment, and to a method for monitoring the dissemination of cancer cells from aggregated cancer cells, and the epithelial-mesenchymal transition, migration, invasion, and metastasis of cancer cells. Specifically, it was verified that, in the case where a cell line or a spheroidically aggregated cell line, in which KRS has been regulated to be expressed or unexpressed, was constructed by using various colorectal cancer cells including HCT116 cell line and then cultured in a two-dimensional environment, the incomplete epithelial-to-mesenchymal transition phenotype (incomplete ECM phenotype) was induced in the cell line inhibiting KRS expression, and the inhibition of KRS expression inhibited cell-extracellular matrix (ECM) adhesion and cell-ECM signaling activity. In addition, it was verified that, in the case where the constructed spheroid cell line was cultured in an aqueous environment or a three-dimensional collage gel culture environment, the inhibition of KRS expression induced cells into mesenchymal cells but failed to reach the disintegration of cell-cell adhesion; inhibited the cell-ECM adhesion and the related signaling activity, causing the inhibition of the dissemination of cells from spheroid cells cultured in a three-dimensional collagen gel culture environment; and failed to induce the dissemination of cells through TGFβ1 present in the cellular microenvironment. Thus, the present invention can be used as a method for screening a cancer metastasis inhibitor and a method for monitoring the migration, invasion and metastasis of cancer cells, and will be useful as one of the screening methods capable of creating low-cost, high-efficient added value at the time of pre-clinical tests required for drug development.

The invention provides application of a non-nucleoside reverse transcriptase inhibitor dapivirine (TMC120) to preparation of drugs used for treating glioblastoma. According to the invention, in-vitro experiments are carried out to detect cytotoxic effect of dapivirine on a human glioblastoma cell strain U87 and influence of dapivirine on the migration and invasion ability of U87, on proliferation, apoptosis and autophagy of U87 cells, on expression of epithelial-mesenchymal transition-associated proteins and on signal channels in the U87 cells, so the potential antineoplastic effect of dapivirine is preliminarily revealed; and the in-vivo anti-glioblastoma activity of dapivirine is confirmed via a nude-mouse in-vivo transplantation tumor model. Dapivirine provided by the invention can be used for development of novel anti-glioblastoma drugs.

The invention aims to provide a miRNA and an application of miRNA in preparation of a product for diagnosing and treating posterior capsule opacification. The miRNA is miR-204-5p and the RNA sequence is SEQ ID NO:1. A miRNA gene product can be used for adjusting the expression of an SMAD4 gene, blocking a TGF (Transforming Growth Factor)-beta/Smads signal channel and inhibiting epithelial-mesenchymal transition (EMT), and has the potential of preparing the diagnosing and treating product for the posterior capsule opacification PCO.

Provided is a gastric cancer cell line derived from a mouse deficient in E-cadherin and p53, and a use thereof. The E-cadherin- and p53-deficient, murine-derived gastric cancer cell line of the present invention was confirmed to have histopathological characteristics similar to those of human gastric cancer, have an epithelial mesenchymal transition (EMT) phenotype and an activated β-catenin pathway, and promote cancer growth in vivo due to potential of carcinogenesis, and thus the gastric cancer cell line of the present invention can be effectively used for the evaluation of the activity of new anticancer drugs and the development of metastasis inhibitors.