74 results about "Epithelial–mesenchymal transition" patented technology

AnnexinA2 (ANXA2), a member of the Annexin family of calcium-dependent, phospholipid binding proteins, is one of a panel of identified antigens recognized by the post-vaccination sera of patients who demonstrated prolonged disease-free survival following multiple vaccinations. AnnexinA2 is abundantly expressed in pancreatic adenocarcinomas and cell surface / membrane AnnexinA2 increases with the progression from premalignant lesions to invasive pancreatic adenocarcinomas. The cytoplasmic to cell surface translocation of AnnexinA2 expression is critical for pancreatic cancer cell invasion. In addition, phosphorylation of AnnexinA2 at Tyrosine 23 is important for its localization to the cell surface and for the invasion of pancreatic cancer cells. Finally, loss of AnnexinA2 leads to the loss of the Epithelial-Mesenchymal Transition.

AnnexinA2 (ANXA2), a member of the Annexin family of calcium-dependent, phospholipid binding proteins, is one of a panel of identified antigens recognized by the post-vaccination sera of patients who demonstrated prolonged disease-free survival following multiple vaccinations. AnnexinA2 is abundantly expressed in pancreatic adenocarcinomas and cell surface / membrane AnnexinA2 increases with the progression from premalignant lesions to invasive pancreatic adenocarcinomas. The cytoplasmic to cell surface translocation of AnnexinA2 expression is critical for pancreatic cancer cell invasion. In addition, phosphorylation of AnnexinA2 at Tyrosine 23 is important for its localization to the cell surface and for the invasion of pancreatic cancer cells. Finally, loss of AnnexinA2 leads to the loss of the Epithelial-Mesenchymal Transition.

The present invention provides methods of diagnosing a cancer or providing a prognosis for a cancer by analyzing the level of expression of a marker that is a downstream target of N-cadherin.

The invention provides novel pharmaceutical purposes of jaceosidin and specifically relates to application of jaceosidin in prevention or treatment of pulmonary fibrosis, wherein through inhibition of pulmonary epithelial-mesenchymal transition, pulmonary vascular endothelial-mesenchymal transition and propagation of fibroblasts, growth and development of pulmonary fibrosis are inhibited, so prevention or treatment of pulmonary fibrosis is realized. In the above-mentioned application, the dosage range of applied jaceosidin is 20 to 1000 mg, preferably, 20 to 500 mg.

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 invention discloses an application of hesperidin in preparation of a medicament for preventing and / or treating pulmonary fibrosis diseases. By virtue of experimental verification, the hesperidin can achieve an effect of preventing and treating pulmonary fibrosis by inhibiting lung fibroblast proliferation, inhibiting epithelium-mesenchyme conversion of alveolar epithelial cells and inhibiting lung fibroblast activation, so that the hesperidin can achieve a new application in preparation of the medicament for preventing and / or treating the pulmonary fibrosis diseases. The application relates to various medicament dosage forms such as capsules, drop pills, aerosol preparations, spraying agents, tablets, granules and injections prepared from the hesperidin. Moreover, the application also relates to a composition, which is formed by taking the hesperidin as a main component, for preventing and treating the pulmonary fibrosis.

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 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 discloses a capturing method and a capturing kit for circulating tumor cells. The capturing method includes the following steps: S1, using lymphocyte separation solution to separate cells from peripheral blood to obtain albuginear cells; and S2, using an EpCAM antibody and a Vimentin antibody to capture circulating tumor cells in the albuginear cells. According to the technical scheme of the invention, by adding an interstitial marker (Vimentin) antibody and mixing the Vimentin antibody with the EpCAM antibody to capture CTCs (Circulating Tumor Cells), both conventional epithelial CTCs and more dangerous CTCs with EMT (Epithelial-Mesenchymal Transition) can be captured, the capture efficiency can be greatly improved, and the detection rate of CTCs can be improved.

The invention discloses an application of protein arginine methyltransferase 7 in cancer cell metastasis. The invention also discloses an application of the protein arginine methyltransferase 7 in preparation of a product for promoting epithelial-mesenchymal transition. The invention proves that PRMT7 (protein arginine methyltransferase 7) has extremely high expression in breast cancer tissues and can induce breast cancer cells to generate EMT (Epithelial Mesenchymal Transition) and promote intrusion and migration of the breast cancer cells. The EMT can be inhibited by interfering the PRMT7, the intrusion and migration capacity of the breast cancer cells can be reduced, and the PRMT7 can serve as a target to be applied to cancer therapy.

The invention relates to the field of medicine biology, wherein a liver-specific MEN1 gene knocked out mouse model is established to research effects of menin in liver cells, and results show that MEN1 gene provides important effects in EMT inhibition (epithelial-mesenchymal transition of liver cells) and glycolipid metabolism regulation. In addition, the MEN1 gene can be adopted for preparing and screening anti-hepatic fibrosis and anti-fatty liver drugs so as to provide valuable clues and directions for clinical targeted therapy.

The inventors of the present invention have surprisingly discovered that EGFR expression in nonmetastatic breast cancer patients with CK-negative CTCs could induce EMT process. A simultaneous detection of both EGFR and EMT markers (VIM and Slug) in CTCs might improve prognostic or predictive information in patients with operable breast cancer.

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 relates to a retinal pigment epithelium epithelial-mesenchymal transition model and application thereof. After being digested with pancreatin, ARPE-19 (acute retinal pigment epitheliitis 19) cells are transferred to a serum-free DMEM-F12 medium containing N2 and non-essential amino acids and are cultured in a Petri dish, and the retinal pigment epithelium epithelial-mesenchymal transition model is acquired. The model is usable for researching a molecular mechanism of retinal pigment epithelium to which epithelial-mesenchymal transition occurs and finding intervened targeting of epithelial-mesenchymal transition.

The invention discloses an application of parthenolide in preparation of a lung cancer treating drug. EMT (epithelial-mesenchymal transition) of lung cancer cells is reversed through parthenolide, so that growth, invasion or metastasis of the lung cancer cells is inhibited. Embodiments of the invention comprise experimental study including an MTT test, Transwell, a scratch test, immunofluorescence and the like on cells and animals, and results show that parthenolide can reverse EMT of the lung cancer cells, so that parthenolide inhibits invasion and metastasis of the lung cancer cells of small cell lung cancer and non-small cell lung cancer and can have a remarkable effect on tumor cancer treatment.

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 discloses a waveform protein response type wash-free fluorescent probe as well as a preparation method and application thereof. The probe comprises a peptide fragment with affinity to waveform protein, an aggregation-induced luminescent type fluorescent group and a connecting group for connecting the peptide fragment with the fluorescent group. The probe can specifically generate thefluorescence response to the waveform protein and has advantages of high simplicity and convenience in operation, washing prevention, low detection cost, high specificity, high accuracy and the like.The probe serving as a detection reagent can be used for specific detection of epithelial-mesenchymal transition type tumor cells and tumor tissues with high sensitivity.

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.

MEHP treatment significantly increases the migration and invasion ability of tumor cells, and the results show that MEHP can induce epithelial-mesenchymal transition of ovarian cancer cells. SKOV3 cells treated by the MEHP with a concentration of 500nM are subjected to transcription group sequencing by a high-throughput sequencing method, the sequencing result is analyzed, and 39 confirmed long-chain non-coding RNAs are screened out; and in the differentially-expressed 39 lnc RNAs, the results show that linc00205 plays an important role in the ovarian cancer cell migration, invasion ability improvement and epithelial-mesenchymal transition induced by the MEHP.

The invention discloses an application of miR-21 in the regulation of ionizing radiation induced epithelial-mesenchymal transition. The invention provides an application of an miR-21 related biomaterial in the preparation of a product for regulating the radiation-induced epithelial-mesenchymal transition. The miR-21 related biomaterial is miR-21, or a substance capable of promoting the expressionof miR-21, or a substance capable of inhibiting the expression of the miR-21; and the miR-21 is mature miR-21 or precursor miR-21. It is disclosed that ionizing radiation induces the increase in the expression of the miR-21 in lung epithelial cells (A549 and Beas-2B), and the induced miR-21 inhibits the expression of a target protein PTEN and activate an Akt pathway in order to promote the occurrence of EMT. Therefore, the miR-21 can become a new biomarker and therapeutic target for treating radiation-induced pulmonary fibrosis.

The object of the present invention is to provide an evaluation method capable of accurately determining a metastasis of cancer, the stage of cancer progression, or the malignancy of cancer.The object can be solved by a method for detecting the degree of malignancy of each of the circulating tumor cells, characterized by the following steps: (a) bringing an epithelial cell-binding component, which specifically binds to a marker molecule expressed on epithelial cells and is fluorescently-labeled or luminescent enzyme-labeled, and a mesenchymal cell-binding component, which specifically binds to a marker molecule expressed on mesenchymal cells and is fluorescently-labeled or luminescent enzyme-labeled, into contact with a sample that possibly contains circulating tumor cells, (b) detecting a fluorescence signal or a luminescence signal of the epithelial cell-binding component and a fluorescence signal or a luminescence signal of the mesenchymal cell-binding component of each of the cells, and (c) determining the degree of epithelial-mesenchymal transition of circulating tumor cells based on the signal amount of the epithelial cell-binding component (E) and the signal amount of the mesenchymal cell-binding component (M).

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.