17 results about "Epithelial–mesenchymal transition" patented technology

The invention belongs to the technical field of application of plant exosomes, and discloses a plant-derived hybrid exosome and application of the plant-derived hybrid exosome in pulmonary fibrosis resistance. After screening a proper proportion, the obtained hybrid exosome has an obvious treatment effect on a mouse with pulmonary fibrosis induced by bleomycin, and the treatment effect is specifically shown as follows: (1) the hybrid exosome can obviously relieve lung inflammatory cell infiltration of the model mouse, protect a pulmonary alveolar structure and relieve the degree of pulmonary fibrosis; (2) the hybrid exosome can effectively reduce the expression levels of TNF-alpha, IL-1beta and IL-6, and can effectively slow down the pulmonary fibrosis process; the lung tissue inflammation is inhibited; and (3) the hybridized exosome inhibits the generation of ECM (extracellular matrix) and inhibits epithelial mesenchymal transition, so that the anti-fibrosis effect is achieved. The plant source hybrid exosome prepared by the invention is wide in plant source, simple in exosome preparation process and low in cost, and provides new possibility for treating pulmonary fibrosis.

Lung fibroblast play an important role in lung cancer tumor microenvironment (TME). Senescence is involved in the pathophysiology of tumorogenesis. analyze how sPLA2 influenced lung cancer cell malignant properties. The inventors show that secreted PLA2 XIIA (sPLA2 XIIA) play a key role in lung cancer cell malignant properties. They demonstrate that sPLA2 XIIA increases the proliferation, the migration and organoid growth of both lung cancer cell lines (NCI and A549). Indeed, they shows that sPLA2 XIIA induces notably the epithelial mesenchymal transition (EMT), which is involved in the invasion of cancer cells and in the formation of metastasis. They also demonstrate that the effect of sPLA2 XIIA is mediated in particular by syndecan 1 and 4. Taken altogether, these data define sPLA2 XIIA as a circulating biomarker of poor prognosis in lung cancer and establish a requirement for sPLA2 XIIA inhibition for the treatment or prevention of cancer, especially lung cancer in the COPD patients.

The invention relates to the technical field of biomedicine detection, and discloses a tumor cell marker detection system for predicting the activation state of intracellular protein kinase. Comprising a marker detection module used for qualitatively detecting epithelial cell markers, mesenchymal cell markers, cell polarity markers and extracellular matrix related markers in tumor cells; the data processing module is used for performing cross validation on an epithelial cell marker, a mesenchymal cell marker, a cell polarity marker and an extracellular matrix related marker; the dynamic weighting module is used for performing dynamic weighting on different markers based on a complex system theory, and endowing epithelial cadherin with a higher weight; and the judgment module is used for determining whether epithelial intercellular substance transformation occurs or not according to the dynamically weighted marker data, and predicting the activation state of intracellular phosphoinositide 3-kinase alpha and the invasiveness of tumor cells based on the determination result of the epithelial intercellular substance transformation.

The present invention relates to a method of inducing mesenchymal-epithelial transition (MET) in a basal-like (or mesenchymal-like) cancer cell by contacting the cancer cell with an inducer of mesenchymal-epithelial transition for a time and under conditions sufficient to induce MET in the cell. Additionally, there is also provided a method of inhibiting epithelial-mesenchymal transition (EMT) of a cancer in a subject, the method comprising administering an inhibitor or regulator of lipid metabolism for a sufficient time and under conditions to inhibit epithelial mesenchymal transition (EMT) of the cancer in the subject.

The invention discloses a circular RNA (Ribonucleic Acid) hsacirc0013599 and application of the circular RNA hsacirc0013599 in preparation of a medicine for treating cleft lip and palate, the hsacirc0013599 can participate in generation and development of CP (Clear Protein) by promoting an epithelial mesenchymal transformation process, and the hsacirc0013599 plays a molecular function through miRNA (Micro Ribonucleic Acid) and mRNA (Messenger Ribonucleic Acid) and participates in regulating the balance of proliferation and migration in a related signal channel in an HEPM (High Efficiency Particulate Matrix) embryonic development process to regulate the development of a cleft lip and palate. The circular RNA hsacirc0013599 has the advantages that the circular RNA hsacirc0013599 can be used as a marker for early screening, diagnosis and treatment of CP, the circular RNA hsacirc0013599 has a good application prospect in medicines for regulating and controlling HEPM behaviors and epithelial-mesenchymal transition, and a research basis is provided for preparing medicines for early screening of cleft lip and palate and treating cleft lip and palate.

The application discloses an IGF2BP2-m6A-VCAN-TLR2 signal axis in the preparation of a drug for treating intrahepatic cholangiocarcinoma lymphatic metastasis. In view of the problems of unknown intrahepatic cholangiocarcinoma lymphatic metastasis mechanism and lack of effective target, the application finds and verifies a new pathway that from insulin-like growth factor 2 mRNA binding protein 2, m6A modification regulates the expression of multi-functional proteoglycan, and then activates Toll-like receptor 2 signal, promotes macrophage secretion of vascular endothelial growth factor C and drives lymphatic metastasis. Based on this, the application provides an inhibitor targeting the signal axis, in particular, a small molecule compound 8010-8498. Experiments show that the compound can significantly inhibit cholangiocarcinoma cell migration, invasion and epithelial mesenchymal transition, reduce macrophage secretion of vascular endothelial growth factor C, and effectively inhibit tumor growth and lymphatic metastasis in a naked mouse popliteal lymph node metastasis model and a spontaneous cholangiocarcinoma model. The compound presents a synergistic effect in combination with gemcitabine and cisplatin.

This invention discloses the use of LAPTM5 in the preparation of drugs regulating renal tubular epithelial-mesenchymal transition (EMT). Through bioinformatics analysis and multi-level experimental verification, this invention found that LAPTM5 is significantly upregulated in an aging kidney model and is positively correlated with renal aging and the severity of fibrosis. Mechanistic studies show that LAPTM5 interacts with the deubiquitinating enzyme USP10 and promotes its lysosomal degradation, weakening the deubiquitination effect of USP10 on PTEN. This leads to proteasomal degradation of PTEN via the K48-linked polyubiquitination pathway, thereby relieving PTEN's inhibition of the PI3K / AKT / mTOR signaling pathway, inhibiting autophagy activity, promoting renal tubular epithelial-mesenchymal transition, and accelerating the process of renal fibrosis. At the cellular level, PTEN overexpression can rescue LAPTM5-induced EMT; in animal models, the PTEN agonist matrine significantly improves D-galactose-induced renal fibrosis in aging mice and protects renal function by restoring autophagy.

Provided herein are markers and methods to improve management of renal cancer. In some embodiments, the disclosure relates to a panel of biomarkers and use thereof to improve management of renal cell carcinoma, including clear cell renal cell carcinoma.

The present invention relates to a method for producing a human salivary organoid-based epithelial-mesenchymal transition and fibrosis model and a use thereof. The invention provides an epithelial-mesenchymal transition and fibrosis model produced by culturing organoids based on epithelial cells derived from human salivary gland tissue and treating same with activin A. In addition, the epithelial-mesenchymal transition and fibrosis model can be used for screening novel therapeutics.

The invention provides a video display terminal related dry eye diagnostic biomarker and a therapeutic drug based on epithelial-mesenchymal transition and fibrosis. By studying functional transformation of epithelial cells in the VDT-related dry eye, epithelial-mesenchymal transition of ocular surface epithelial cells in the VDT-related dry eye is revealed, and fibroblast characteristics and proinflammatory characteristics are presented in an acute stage of a disease course, so that the acute stage and the chronic stage of the VDT-related dry eye are distinguished. Disclosed are biomarkers for diagnosing or monitoring the efficacy of a treatment for VDT-related dry eye, and preparation of reagents or kits for diagnosing, monitoring the efficacy of a treatment for a VDT-related dry eye, or differentiating acute and chronic progresses in VDT-related dry eye patients based on the markers. Besides, intervention aiming at the epithelial-mesenchymal transition and fibrosis process is an effective strategy for relieving VDT-related dry eye inflammation and improving ocular surface injury, and a potential intervention direction and prospect are provided for clinical treatment of VDT-related dry eye.

Methods for identifying and selecting algorithms usable for detecting tumors and / or cancers in patient samples are provided. In some embodiments, the methods include determining gene expression levels of one or more of FGFR1OP2, CDH1, TP53, PIK3CA, S100A8, FAXDC2, CLEC12A, DMTN, MUC1, PSPH, MALAT1, and MKI67 present in a biological sample isolated from the subject that has one or more tumor educated cells that have been contacted directly or indirectly by the tumor and / or the cancer. Disclosed methods include, but are not limited to, generating gene expression profiles predictive of diseases and / or disorders, inhibiting gene expression changes resulting from initiation and / or progression of diseases and / or disorders, inhibiting proliferation and / or survival of target cells, inhibiting epithelial mesenchymal transition (EMT), inhibiting platelet aggregation, and inhibiting loss of immune cell targeting ability, among others. Also provided are systems for use in the presently disclosed methods.

The application discloses a pancreatic cancer JAK2 and STAT3 dual-target inhibitor containing a phenoxy acetic hydrazine compound and application thereof, and the dual-target inhibitor comprises a compound containing a phenoxy acetic hydrazine structure. The dual-target inhibitor comprises a pharmaceutically acceptable salt. The pancreatic cancer JAK2 and STAT3 dual-target inhibitor containing the phenoxy acetic hydrazine compound is applied to the preparation of a drug for treating pancreatic cancer. The drug has a new use in treating pancreatic cancer by inhibiting tumor proliferation, migration and invasion, angiogenesis, epithelial mesenchymal transition, blocking a cell cycle and promoting cell apoptosis. The pharmaceutical preparation of the drug composition comprises tablets, capsules, syrup, suspensions and injections. A drug for treating pancreatic cancer comprises the pancreatic cancer JAK2 and STAT3 dual-target inhibitor containing the phenoxy acetic hydrazine compound and a pharmaceutically acceptable carrier. The application has the beneficial effect that the pancreatic cancer JAK2 and STAT3 have a better inhibiting effect, the experimental results show that the inhibiting effect is good, the application prospect is wider, and the safety is better.

The invention discloses a DNA tetrahedron-based epithelial mesenchymal transformation probe and application thereof, and relates to the technical field of tumor detection, the DNA tetrahedron-based epithelial mesenchymal transformation probe comprises a DNA tetrahedron with extended chains at vertexes, and the four vertexes of the DNA tetrahedron are respectively loaded with a hairpin chain; the novel DNA probe provided by the invention is formed by loading four DNA chains on a DNA tetrahedron with an extended chain at the vertex, and can simultaneously perform specific response with miRNA-200c and miRNA-221, so that the process of tumor cell epithelial mesenchymal transition can be represented, and whether tumor cells appear and are transferred or not can be conveniently judged.

Disclosed herein is a therapeutic agent for fibrosis comprising an ICAM-1 inhibitor. It has been found that inhibition of the function of ICAM-1 in a tissue that has been affected by fibrosis restores a fibrotic tissue to a normal tissue, thereby treating fibrosis, and the therapeutic mechanism has been clarified by studies. The therapeutic agent for fibrosis containing the ICAM-1 inhibitor can inhibit ICAM-1-mediated signaling, and thus inhibit epithelial mesenchymal transition (EMT) of tissue epithelial cells in which ICAM-1-mediated signaling is involved and / or accumulation of extracellular matrix in which ICAM-1-mediated signaling is involved. The fibrosis therapeutic agent containing the ICAM-1 inhibitor has a therapeutic mechanism for inhibiting the induction of EMT in tissue epithelial cells, preventing differentiation into myofibroblasts by inhibiting the activity of local fibroblasts, and / or reducing myofibroblasts by directly acting on myofibroblasts.

The invention relates to the field of biological medicines, and discloses application of icariside II in preparation of a medicine for treating chronic asthma. The icariside II plays a role in treating chronic asthma by improving lung functions, relieving airway inflammation, relieving airway remodeling and inhibiting lung epithelium-mesenchymal transition. The invention discloses the new application of icariside II in treating chronic asthma for the first time, and provides a brand-new drug choice with multi-target treatment potential for clinical treatment of chronic asthma through a multi-way synergistic effect.

The present invention relates to a method for the prevention, improvement, or treatment of cancer patients, particularly patients with EMT (Epithelial mesenchymal transition) subtype cancer. In cancer patients in whom the expression level of the GLS (Glutaminase) gene or the protein encoded by it is increased, when PHGDH, SHMT, and MTHFD2 inhibitors are administered in combination, 1C metabolism is more effectively inhibited, and there is a synergistic effect in inhibiting the proliferation of cancer cells in patients with intractable cancer that is difficult to treat due to recurrence, metastasis, and resistance to anticancer drugs, thereby enabling very effective treatment of cancer. Furthermore, by measuring the expression levels of the GLS gene or the protein encoded by it, information regarding personalized treatment methods can be provided to individual patients from the early stages, thereby increasing the success rate of treatment.

The invention belongs to the technical field of biological medicines, and particularly relates to application of fucoxanthin in preparation of a medicine for preventing and treating chemotherapy-induced stomatitis. Experiments show that the fucoxanthin has a protective effect on chemotherapeutic drugs and LPS-induced stomatitis, and specifically, the fucoxanthin has a protective effect on the stomatitis induced by the chemotherapeutic drugs and the LPS-induced stomatitis, and the expression quantity of barrier proteins Occludin and ZO-1 is increased; and the content of epithelial mesenchymal transition (EMT) related protein is reduced. The fucoxanthin is high in safety, wide in source, low in cost and very suitable for being applied to prevention and treatment of stomatitis. The invention not only provides a new drug source for the treatment of stomatitis, but also opens up a new field for the application of the fucoxanthin.