34 results about "P53 expression" patented technology

In fibrotic lung fibroblasts, basal levels of p53 protein (and miR-34a) are markedly suppressed, leading to reduced p53-mediated inhibition of uPA and uPAR, or concurrent induction of PAI-1. These changes contribute to excessive FL-fibroblast proliferation and production of extracellular matrix (ECM), and, therefore, pulmonary fibrosis. These processes are reversed by treating the cells, and treating subjects suffering from idiopathic pulmonary fibrosis (IPF) with the small organic molecule nutlin-3a (NTL) or with a peptide, CSP-4 (SEQ ID NO:1), or variants or derivatives or multimers of this peptide, which increase p53 levels by inhibiting MDM2-mediated degradation of p53 protein. Use of these compounds serves as a new approach to the treatment of IPF, they restore p53 expression and p53-mediated changes in the uPA-fibrinolytic system in FL-fibroblasts and restrict production and deposition of ECM.

During lung injury, p53 expression increases, inducing plasminogen activator inhibitor-1 (PAI-1) while inhibiting expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR), resulting in apoptosis of lung epithelial cells (LECs). In the bleomycin lung injury model, p53 and PAI-1 are induced while uPA and uPAR are inhibited. A 20 residue peptide DGIWKASFTTFTVTKYWFYR termed PP-1 (the Cav-1 scaffolding domain) or peptide NYHYLESSMTALYTLGH, termed PP-2, protected LECs from bleomycin-induced apoptosis in vitro and in vivo and prevented subsequent pulmonary fibrosis by attenuating lung epitheilial damage. Pharmaceutical compositions, peptide multimers and deliverable polypeptides comprising the above peptides are dislcosed. The peptides and functional variants, peptide multimers, cell-targeted polyepeptides and pharmaceutical compositions are used in methods for inhibiting apoptosis of injured or damaged lung epithelial cells and for treating acute lung injury and consequent pulmonary fibrosis.

The present invention relates to a method for maintaining the increased intracellular p53 level, induced by a platinum-based anticancer drug, and an application thereof and, more specifically, to a method for maintaining the increased intracellular p53 level in cells by administering a platinum-based anticancer drug and siRNA to ubiquitin ligase for p53 to a subject in need thereof in combination and sequentially, and a composition for promoting cancer cell apoptosis using the same.According to the method of the present invention, the increased intracellular p53 expression level can be maintained for a long period of time in spite of the treatment with a low-concentration platinum-based anticancer drug, thereby effectively inducing the apoptosis of cancer cells and minimizing the drug side effect caused by the administration of the platinum-based anticancer drug, and thus the present invention can be favorably used in the prevention of cancer or the development of cancer medicines.

The invention provides, inter alia, methods for treating vascular deficiencies, including those in diabetic subjects, by transplanting endothelial progenitor cells with transiently reduced p53 expression.

It has been demanded to improve the poor solubility of curcumin to develop an anti-tumor compound capable of inhibiting the growth of various cancer cells at a low concentration. Thus, disclosed is a novel synthetic compound, a bis(arylmethylidene)acetone, which has both of an excellent anti-tumor activity and a chemo-preventive activity. A bis(arylmethylidene)acetone (i.e., a derivative having a curcumin skeleton) which is an anti-tumor compound and has a chemo-preventive activity is synthesized and screened. A derivative having enhanced anti-tumor activity and chemo-preventive activity can be synthesized.

The invention is based on a finding that silencing CIP2A (KIAA1524) gene sensitizes cancer cells for apoptosis-inducing activity of certain small molecule chemotherapeutic agents. Thus, the invention is directed to a respective combination therapy, sensitization method and pharmaceutical compositions. The invention further relates to a method of selecting cancer therapy for a subject on the basis of CIP2A and p53 expression and / or protein activity in a sample obtained from said subject.

The invention provides diagnostic, prognostic, and therapeutic uses for detecting COP1 overexpression in a variety of cancers. The methods and uses can further include detecting p53 expression. The invention also provides reagents and kits for use in screening for test compounds that interfere with COP1 and p53 binding.

The invention is based on a finding that silencing CIP2A (KI-AA1524) gene sensitizes cancer cells for apoptosis-inducing activity of certain small molecule chemotherapeutic agents. Thus, the invention is directed to a respective combination therapy, sensitization method and pharmaceutical compositions. The invention further relates to a method of selecting cancer therapy for a subject on the basis of CIP2A and p53 expression and / or protein activity in a sample obtained from said subject.

The invention relates to the field of biological medicine, in particular to a cell strain capable of inducing and realizing dual-stabilization of P53 expression and a construction method and application thereof. As for the cell strain capable of inducing and realizing the dual-stabilization of the P53 expression, the cell strain U-2OSE6tet6 was collected in China Center for Type Culture Collection on August 12, 2010, and the collection number is CCTCC No: C201075. Experiments prove that the cell strain U-2OSE6tet6 capable of inducing and realizing the dual-stabilization of the P53 expression can indirectly change the P53 content in U-2OSE6tet6 cells by regulating the expression of an E6 gene through doxycycline, and provide an experimental platform for studying relevant action mechanism of the P53 of screening medicaments for treating osteosarcoma.

The invention discloses an application of promoting ATG5-ATG12 conjugation and enhancing cell autophagy by removing p53 protein. First, the mechanism of p53 protein inhibiting cell autophagy is disclosed, and it is found that after p53 protein is increased, the key regulatory protein ATG5 and cell autophagy The conjugation of ATG12 is significantly weakened; by removing p53 protein, the inhibition of p53 protein on ATG5-ATG12 conjugation is reduced, thereby restoring the process of autophagy; the present invention proves that the mechanism of p53 inhibiting autophagy is that p53 inhibits autophagy by binding to ATG12 The conjugation of ATG12-ATG5 can promote the process of autophagy by removing p53 protein, making the inhibition of p53 expression or the removal of p53 protein a potential drug target for relieving autophagy inhibition and promoting autophagy.

The present invention relates to a method for maintaining the increased intracellular p53 level, induced by a platinum-based anticancer drug, and an application thereof and, more specifically, to a method for maintaining the increased intracellular p53 level in cells by administering a platinum-based anticancer drug and siRNA to ubiquitin ligase for p53 to a subject in need thereof in combinationand sequentially, and to a composition for promoting cancer cell apoptosis using the same. According to the method of the present invention, the increased intracellular p53 expression level can be maintained for a long period of time in spite of the treatment with a low-concentration platinum-based anticancer drug, thereby effectively inducing the apoptosis of cancer cells and minimizing the drugside effect caused by the administration of the platinum-based anticancer drug, and thus the present invention can be favorably used in the prevention of cancer or the development of cancer medicines.

The present invention relates to a pharmaceutical composition for preventing or treating tuberculosis comprising compound (K279-1558) as an active ingredient. Compound (K279-1558) which is an active ingredient of the present invention has an effect of inhibiting the proliferation of M. tuberculosis by inducing apoptosis of macrophages infected with tuberculosis through the overexpression of p53. Therefore, the method of the present invention comprising said compound as an active ingredient could be usefully used for preventing or treating tuberculosis.

A kind of recombinant gene medicine of adenovirus vector and gene p53 which can treat proliferative diseases is a confusion sequence constructed from adenovirus vector and human tumor inhibition gene p53 expression kit. In the present invention, we made homologous recombination of adenovirus vector with human gene p53 in procaryotic cells (E. coli), then obtained the recombinant gene medicine of adenovirus vector and human gene p53 expression kit. The human p53 gene expression kit is a characteristic sequence consisting of promoter-p53 cDNA-polyadenine nucleotide. The medicine can be used to prepare clinic gene therapeutic products for treating proliferative disease such as cheloid.