47 results about "Metastasis Suppression" patented technology

The invention relates to an application of a PNO1 inhibitor to preparation of esophagus cancer treatment medicines, belongs to the field of biopharmaceutical research, and particularly relates to an application of a PNO1 inhibitor to preparation of esophagus cancer treatment medicines. The inventor firstly finds that the PNO1 can be used as an esophagus cancer treatment target point. The PNO1 inhibitor can restrain the proliferation rate of esophagus cancer cells, can restrain the cloning and forming capacity of the esophagus cancer cells, can promote esophagus cancer apoptosis, can restrain esophagus cancer cell migration, can restrain esophagus cancer cell transfer, and can restrain esophagus cancer cell invasion and transfer, so as to treat esophagus cancer, and a new direction is opened up for treatment of esophagus cancer.

The invention discloses a method for inhibiting the growth and metastasis of solid tumor cells and a special pharmaceutical composition, and belongs to the field of animal cell proliferation and transformation. When ovarian cancer HEY cells or breast cancer MDA-MB-231 cells are induced, a culture medium is replaced after acting in high-concentration CoCl2, and after the cells are recovered, the treatment is repeated twice to obtain a sufficient number of cells with high invasion and metastasis ability; and the obtained cells are cultured in a culture medium without CoCl2, then the removed culture medium is added with a pharmaceutical composition prepared from dimethyl sulfoxide, dexamethasone, rosiglitazone, 3-isobutyl-1-methylxanthine for in-vitro induction, and when obvious lipid droplets are formed in tumor cell plasma, it indicates that the tumor cells have adipose differentiation. The method is designed to induce the tumor cell adipose differentiation and the purpose of inhibitingtumor cell growth is achieved. It is confirmed by animal experiments that the method is expected to be used for clinical treatment and metastasis inhibition of human solid tumors.

The present invention provides a therapeutic agent for a tumor, particularly a therapeutic agent for drug-resistant cancer, an agent for suppression or prophylaxis of tumor metastasis, and an agent for suppression or prophylaxis of cancer recurrence, containing a nucleic acid containing miR27b or a nucleotide having a nucleotide sequence having an identity of 70% or more with the nucleotide sequence shown by SEQ ID NO: 1 and having a function equivalent to miR27b.

The invention relates to RNA-binding protein PNO1 capable of being used as a lung cancer diagnosis target and treatment target, and particularly discloses overexpression of the RNA-binding protein PNO1 in lung cancer cells. Overexpression of the RNA-binding protein PNO1 in the lung cancer cells can promote proliferation of the lung cancer cells, and is related to short prognosis survival time of lung cancer patients. By reducing expression of the PNO1, growth and metastasis of the lung cancer cells are inhibited, and apoptosis of the lung cancer cells is increased, so that inhibition of expression of the PNO1 represents a novel strategy for treating lung cancer.

Disclosed is a natural compound, Oblongifolin C, isolated from a natural plant comprising Garcinia species such as Garcinia yunnanesis Hu, for its effects of anti-migration and anti-invasion against cancer and its use as an anticancer drug. The treated cancers comprise cervical cancers and esophageal cancers. The cancer treatment comprises inhibition of cancer metastasis and inhibition of autophagic flux.

The present invention relates to gene therapy for the treatment of tumors. The invention more particularly relates to introduction of a gene encoding an anti-angiogenic factor into cells of a tumor, for example with a defective adenovirus vector, to inhibit growth or metastasis, or both, of the tumor. In a specific embodiment, delivery of a defective adenovirus that expresses the amino terminal fragment of urokinase (ATF) inhibited growth and metastasis of tumors. These effects were correlated with a remarkable inhibition of neovascularization within, and at the immediate vicinity of, the injection site. Delivery of a defective adenovirus vector that expresses kringles 1 to 3 of angiostatin inhibited tumor growth and tumorigenicity, and induced apoptosis of tumor cells. The invention further provides viral vectors for use in the methods of the invention.

A novel domain of Aggrus involved in the binding to CLEC-2 was searched for, and monoclonal antibodies recognizing the domain were obtained. The newly found PLAG4 domain is important for Aggrus binding to CLEC-2. Monoclonal antibodies recognizing this region were further developed. The present invention can provide novel Aggrus-CLEC-2 binding inhibitors, platelet aggregation inhibitors, cancer metastasis inhibitors, and tumor growth inhibitors using these antibodies.

The invention related to the use of high-density loss of heterozygosity (LOH) mapping in lung adenocarcinoma to identify intragenic LOH and driver mutations in different domains of ALK resulted in enhanced tumor growth in xenografted mouse. Mutant (H694R and E1384K) ALKs showed activation of Y1604 ALK and downstream AKT, STAT3 and ERK signaling pathways. Increases of oncogenic signalings resulted in enhanced cell proliferation, colony-formation, cell-migration and tumor-growth in xenografted mouse. Western blot and immunohistochemistry analysis using antibody against phospho-Y1604 ALK on 11 lung cancer cell-lines and 263 cancer specimens indicated ALK activation in all lung cancers regardless of tumor stages. Treating mutant-bearing mice with ALK inhibitor WHI-P 154 resulted in tumor shrinkage, metastasis suppression, and improved survival. Hyperphosphorylation of Y1604 ALK occurred early and continuously throughout tumor progression and could be used as a biomarker to detect lung cancer. Oncogenic ALK point mutations could be treatment targets for lung cancer.

The present invention relates to a composition for treatment or metastasis suppression of cancers which includes a p34 expression inhibitor or activity inhibitor as an active ingredient. According to the present invention, the p34 protein knock-down causes monoubiquitination of PTEN and accordingly nuclear localization of PTEN is induced, as a result, an Akt pathway which is related to survival, proliferation, invasive properties and metastatic properties of tumors is inhibited, and thus there is an effect of significantly reducing clonogenic potential and tumor forming potential of various cancer cells which simultaneously express PTEN and NEDD4-1. Consequently, the p34 gene expression inhibitor or p34 protein activity inhibitor according to the present invention can be effectively used as a treatment agent or a metastasis suppression agent for cancers.

The invention discloses a genetically engineered antigen presenting extracellular vesicle, the antigen presenting extracellular vesicle loads a tumor associated antigen and overexpresses an immunomodulatory molecule and a single-chain antibody at the same time, and a vaccine preparation for tumor treatment is prepared based on the antigen presenting extracellular vesicle. Particularly, the compound has outstanding performance in inhibition of tumor metastasis, and has huge potential in serving as a new-generation drug loading platform. The genetically engineered extracellular vesicles constructed by the invention not only maintain the antigen presentation capability, but also target tumor antigens, and regulate solid tumor immune microenvironment so as to effectively activate T cells in tumors to exert anti-tumor activity, and finally realize tumor killing and metastasis inhibition functions.

The invention belongs to the technical field of biological medicine, and relates to application of a VGF gene in treatment of metastatic prostate cancer. The invention discloses application of a VGF gene inhibitor in preparation of prostatic cancer drugs. It is found for the first time that the VGF can promote invasion and metastasis of the prostate cancer, the VGF has higher expression in prostate cancer tissue with higher malignancy degree, and generation and development of the prostate cancer can be inhibited by inhibiting the VGF. A VGF small-molecule inhibitor siRNA is prepared, so that prostatic cancer is treated, metastasis of the prostatic cancer is inhibited, and a PI3K/AKT signal channel is inhibited. The invention provides a new thought for further researching the pathogenesis of prostatic cancer and the function of the VGF gene, and provides a new direction for the development of prostatic cancer drugs.

Provided is a metastasis suppressing agent containing a HSP47 inhibitor.

The present invention relates to a pharmaceutical composition which is for preventing or treating brain cancer and includes at least 99% of a crystal polymorph of tetraarsenic hexoxide a (As₄O₆-a), and to a method for preparing same. A composition according to the present invention exhibits excellent cancer cell proliferation inhibition and metastasis inhibition effects, and thus may be usefully used as an anti-cancer agent.