9 results about "Epithelial–mesenchymal transition" patented technology

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 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 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.