37 results about "Tumour invasion" patented technology

The invention discloses an in vitro model simulating human tumor metastasis. Cells in the model have a tumor high metastasis character. The model is constructed by building of a micro spherical hydrogel support frame by tumor high metastasis cells, building of a tumor cell in vitro metastasis model and identifying of the constructed tumor cell in vitro metastasis model. The model can grow in a three-dimensional culturing cell in a clustering mode, and tumor cell biological behaviors in metastasis can be detected. The model has important value in studying of a clinical tumor metastasis mechanism and controlling of screening of metastasis medicine and can be taken as a technical platform for manufacturing anti-tumor metastasis gene vaccines and building screening of anti-tumor metastasis medicine.

The present invention discloses the tumor invasion and metastasis resisting function and application of venin cysteine proteinase inhibitor, and belongs to the field of biomedicine. Through designing and synthesizing sv-Cystatin cDNA according to 99 amino acid sequences of Chinese cobra venin Cystatin protein, cloning to pPICZ alphaA vector and transforming Pichia yeast, stable and high expression engineering bacterium GS115-sv-Cystatin is screened out. Through further inducing expression and purification, the extracorporeal bioactivity experiment shows that the recombinant sv-Cystatin protein has the functions of inhibiting the activity of papain and inhibiting the tumor cell invasion and metastasis obviously, and so do the intracorporeal experiment. The present invention also constitutes pcDNA-sv-Cystatin eukaryotic expression vector. The present invention has huge application foreground in preventing and treating tumor.

The invention provides an application of shiandra and dibenzocyclooctadiene lignans for preparing medicaments for resisting tumor invasion and metastasis. When the dibenzocyclooctadiene lignans are used for preparing medicaments for resisting tumor invasion and metastasis, a mixture of two or more than two compounds can also be adopted. In the invention, the application of the shiandra and dibenzocyclooctadiene lignans for preparing medicaments for resisting tumor invasion and metastasis has the following beneficial effects: the shiandra and dibenzocyclooctadiene lignans can effectively prevent and control tumor invasion and metastasis and have good clinical application prospects.

The invention generally relates to a microfluidic platforms or “chips” for testing and understanding cancer, and, more specifically, for understanding the factors that contribute to cancer invading tissues and causing metastases. Tumor cells are grown on microfluidic devices with other non-cancerous tissues under conditions that simulate tumor invasion. The interaction with immune cells can be tested to inhibit this activity by linking a cancer chip to a lymph chip.

A method of identifying transcription factors comprising providing cells with a nucleic acid sequence at least comprising a sequence CACCT (SEQ ID NO: ______ ) as bait for the screening of a library encoding potential transcription factors and performing a specificity test to isolate said factors. Preferably, the bait comprises twice the CACCT (SEQ ID NO: ______ ) sequence, more particularly the bait comprises one of the sequences CACCT-N-CACCT(SEQ ID NO: ______ ), CACCT-N-AGGTG(SEQ ID NO: ______ ), AGGTG-N-CACCT(SEQ ID NO: ______ ), or AGGTG-N-AGGTG (SEQ ID NO: ______ ) wherein N is a spacer sequence. The transcription factors identified using the methods of the invention include separated clusters of zinc fingers, such as, for example, a two-handed zinc finger transcription factor. Also, at least one such zinc finger transcription factor, denominated as SIP1, induces tumor metastasis by down regulation of the expression of E-cadherin. Compounds interfering with SIP1 activity can thus be used to prevent tumor invasion and metastasis.

The present invention is based on the finding that the level of KIR expression in a cancer cell is significant with regard to tumor invasion and metastasis. Therefore, the present invention concerns methods and compositions for evaluating cancer in a patient based on KIR protein or mRNA expression. The invention also provides methods and compositions for treating cancer using a KIR inhibitor and methods of screening for KIR inhibitors.

The invention relates to a visualization method for quantifying glioma invasiveness based on a kernel density function, which is a method for quantifying glioblastoma invasiveness established by usinga kernel density estimation algorithm on the basis of Image J software and an R language platform. According to the method, a nuclear density estimation graph of cell nucleus distribution is deducedby utilizing a nuclear density estimation algorithm packaged by an R language ggplot2 packet and an MASS packet and a visualization function. The method can help to effectively judge the invasion condition of the tumor from the pathological section in scientific research work, the tumor nuclear density of each region is counted by utilizing the nuclear density, the invasion trend of the tumor canbe roughly judged from a visual graph, and the tumor invasion ability is reflected from the section.

The invention belongs to the biomedical engineering field, and relates to a trachea substitute and a preparation method therefor. The trachea substitute has a porous and three-dimensional network structure, is a tubular, tegular or Y-type decellularized biomaterial, and comprises biological materials of allogeneic or heterogeneous sources. There are holes on the outer surface and the outer surface is seamed with spiral polyester materials. Experiments show that the trachea substitute has good biocompatibility with tissues, has no antigen interference effects, can perform revascularization and re-epithelization rapidly, has good air impermeability, ductility and elasticity, and can prevent collapse during breath. The trachea substitute can be made into different shapes and specifications, is suitable for tracheal reconstructive operations of tubular trachea substitution, juga molding, tracheal patching and the like. The trachea substitute is especially suitable for post-operation trachea substitution of trachea tumours, trachea trauma, benign tracheal stenosis, tumour invasion, congenital trachea malformation and the like.

The invention discloses a method for predicting malignant tumor metastasis and invasion capacity in vitro, which comprises the following steps of: (a) extracting DNA (Deoxyribonucleic Acid) from surgical incisal margins or tumor-adjacent tissues; (b) detecting the methylating degree of cytimidine in 5'- end CpG island of seroreaction factor gene DNA sequence in DNA obtained in the step (a); and (c) when the seroreaction factor gene DNA sequence with methylated cytimidine in the 5'-end CpG island is detected in the step (b), presuming that the tissue being detected has the capacity of resisting malignant tumor metastasis and invasion. The invention also provides four artificial nucleotide fragments. The inventor of the invention, for the first time, find that the metastasis and invasion capacity of malignant tumors can be rapidly and accurately predicted by detecting whether the seroreaction factor gene DNA sequence with methylated cytimidine in CpG island exists or not in the tissue being detected. Besides, the nucleotide fragments provided in the invention can be used for accurately and rapidly detecting the methylation of cytimidine in the CpG island in the seroreaction factor gene DNA sequence.

The invention provides methods for treating HIF-1α-overexpressing human tumors, inhibiting HIF-1α-overexpressing tumor invasion and preventing tumor metastasis, and / or promoting tumor prophylaxis, using various types of inhibitors against the Hsp90α from the tumors.

The invention discloses application of valproic acid in preparation of a multidrug resistance reversal agent of a lung cancer resistance medicine, and further discloses application of the valproic acid in the preparation of chemotherapeutics sensitizer of lung cancer resistance and a multidrug resistance tumor invasion resisting and transferring medicine. The application of the valproic acid in the preparation of the multidrug resistance reserval agent of the lung cancer resistance medicine verifies that valproic acid has significant function of a cisplatin persister of human lung cancer resistance through experiments, and verifies that the valproic acid can significantly change drug tolerance of a human lung cancer cell to the cisplatin, improve sensitivity of the human lung cancer cell to the cisplatin, and have obvious restraining effect of invasion effect of the persister of the lung cancer cisplatin.

A recombinant fusion protein able to resist against tumor invasion and transfer is composed of the recombinant urokinase fragment and type-2 mutant as plasminogen activator inhibitor. The fusion protein gene cDNA is amplified by PCR method, and is cloned to expression vector to obtain fusion gene expression plasmid, which is used to transform host bacteria. The methanol or temp can induce the expression of said fusion protein. After purified, a high-purity (95%) expression product is obtained.

The invention provides an M1 type macrophage exosome vaccine as well as a preparation method and application thereof. The M1 type macrophage exosome vaccine is characterized in that an exosome vaccine M1Ag-Exos is obtained by enabling M1 type macrophages to uptake a specific tumor antigen Ag and then extracting an exosome of the M1 type macrophages carrying the tumor antigen Ag. According to the M1 type macrophage exosome vaccine, the exosome vaccine capable of adjusting the tumor immune microenvironment is constructed to enhance the immunotherapy efficiency, and polarization of tumor-related macrophages and the remarkable immune activation effect of a tumor vaccine are achieved through the M1 type macrophage exosome; the tumor-related macrophages are polarized into M1 type, so that the macrophages are converted from a state of promoting tumor invasion and metastasis by immunosuppression into a state of supporting tumors by immunity; meanwhile, through immunoregulation on the tumor microenvironment, the tumor vaccine can promote proliferation and activation of T cells more efficiently, and growth and metastasis of the tumors are effectively inhibited.

The invention provides a TIPE3 immunohistochemical detection kit as well as a use method and application thereof, and belongs to the technical field of tumor detection. The research finds that the expression of the TIPE3 in the pancreatic cancer is obviously increased, is closely related to tumor invasion and metastasis potential and is an independent prognosis risk factor of a pancreatic cancer patient, so that the aims of helping to judge the malignant degree of the pancreatic cancer and prognosis of the patient can be fulfilled by detecting the expression of the TIPE3, and the TIPE3 immunohistochemical detection kit is provided. The kit can effectively predict the malignancy degree and metastasis potential of pancreatic cancer, and perform recurrence and metastasis risk grading on pancreatic cancer patients; and meanwhile, the prognosis condition of the patient can be evaluated, so that the survival rate of the pancreatic cancer patient can be improved, an important scientific basis is provided for clinical prevention and treatment of the pancreatic cancer, and therefore, the kit has good clinical application value and social benefits.

The invention relates to CD146 and antibody diagnosis thereof, and an application thereof in treating triple negative breast cancers. For a first time, the invention provides that CD146 is a novel target of triple negative breast cancer, and an anti-CD146 antibody might become a novel targeting medicine for treating the disease. Therefore, the invention provides an application of CD146 or anti-CD146 antibody or a functional form of the antibody in preparing medicines used for diagnosing and / or treating triple negative breast cancers. CD146 molecules are subjected to specific high expression in triple negative breast cancer tissues, and induce the occurrences of transformation of epithelial cell to mesenchymal cell in tumor cells. Therefore, tumor invasion migration is promoted. Therefore, the mechanism for CD146 antibody to treat triple negative breast cancer is mainly that the CD146 antibody inhibits the mesenchymal cell characteristics of triple negative breast cancer, and reduces the metastasis invasion capacity thereof. Compared with common chemotherapy medicines, the anti-CD146 antibody has the advantages of low side effects and clear target. The anti-CD146 antibody does not cause whole-body side effect.

The invention relates to multiple-target fusion protein resistant to tumor invasion and metastasis. The fusion protein has following amino acid sequence structures: RGD peptide-connecting peptide-TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) functional peptides-connecting petide-NGR peptide; the fusion protein has proliferation effect on inhibiting cancer cells of the TRAIL peptides and migration inhibition of the tumor cells of two targeting peptides of GRD and NGR. By comparison, the multiple-target fusion protein is more remarkable in antitumor activity, and resistance to the TRAIL is reversed to a certain extent. The invention further provides an encoding gene of the fusion protein and a pharmaceutical purpose of the fusion protein.

It has been shown that Compound 1 unexpectedly and potently inhibits TIE2 kinase, and that Compound 1 inhibits drug resistance mechanisms in both the tumor and in the surrounding microenvironment through balanced inhibition of TIE2, MET, and VEGFR2 kinases. Thus, Compound 1 provides a single therapeutic agent able to address multiple hallmarks of cancer by inhibiting TIE2, MET, and VEGFR2 kinases in the tumor microenvironment [Hanahan 2011]. Through its balanced inhibitory potency vs TIE2, MET, and VEGFR2, Compound 1 provides an agent which inhibits three major tumor (re)vascularization and resistance pathways (ANG, HGF, VEGF) and blocks tumor invasion and metastasis. Compound 1 exhibits anti-tumor activity alone and in combination with other targeted agents or chemotherapy.

A method of identifying transcription factors comprising providing cells with a nucleic acid sequence at least comprising a sequence CACCT (SEQ ID NO:1) as bait for the screening of a library encoding potential transcription factors and performing a specificity test to isolate said factors. Preferably, the bait comprises twice the CACCT (SEQ ID NO:1) sequence, more particularly the bait comprises one of the sequences CACCT-N-CACCT (a first SEQ ID NO:1 and a second SEQ ID NO:1 separated by N), CACCT-N-AGGTG (SEQ ID NO:1 and SEQ ID NO:3 separated by N), AGGTG-N-CACCT (SEQ ID NO:3 and SEQ ID NO:1 separated by N), or AGGTG-N-AGGTG (a first SEQ ID NO:3 and a second SEQ ID NO:3 separated by N), wherein N is a spacer sequence. The transcription factors identified using the methods of the invention include separated clusters of zinc fingers, such as, for example, a two-handed zinc finger transcription factor. Also, at least one such zinc finger transcription factor, denominated as SIP1, induces tumor metastasis by down regulation of the expression of E-cadherin. Compounds interfering with SIP1 activity can thus be used to prevent tumor invasion and metastasis.

The invention provides a polypeptide-metal cluster probe for specifically recognizing membrane protein of a circulating tumor cell (CTC) and application of the polypeptide-metal cluster probe in quantitative detection, and belongs to the technical field of medical detection. The polypeptide-modified metal cluster probe prepared by the invention contains a metal cluster core and a target peptide which is specifically combined with target cell membrane protein. The prepared polypeptide-metal cluster probe targets the membrane protein expressed by CTC, and a laser ablation inductively coupled plasma mass spectrometry technology is utilized to perform rapid and accurate in-situ quantitative analysis on the peripheral blood CTC target membrane protein of a clinical tumor patient, so that an important reference is provided for tumor invasion and metastasis behaviors, grading and prognosis of the clinical tumor patient.

The invention relates to a cholangiocarcinoma cell medicine target point. The medicine target point is ubiquitin specific protease 8, and the nucleotide sequence is shown as SEQID NO:1 in a sequence table. For the first time, the invention puts forward that USP8 is knocked down, so that proliferation, migration and invasion of cholangiocarcinoma cells can be notably restrained, MMP9 activity achieving important effects on cell adhesion, neoplasm invasiveness and transfer is reduced, and the USP8 is promoted to achieve effect of oncogene for growth and transfer ability of cholangiocarcinoma. New possibility is provided for development of cholangiocarcinoma medicines and cholangiocarcinoma prevention, treatment and prognosis.

The invention relates to the field of cancers, in particular to a biomarker beneficial to liver cancer diagnosis and prognosis, and the change level of the biomarker (transcription activator 4) in a subject sample is beneficial to liver cancer diagnosis of a subject or prognosis of a liver cancer subject. Compared with a traditional biomarker, the ATF4 protein can more comprehensively mark liver cancer cells and has obvious expression difference in liver cancer lesions, the range of the cancer lesions can be confirmed through detection, and the tumor invasion range can be judged more easily; the traditional tumor biomarker Ki67 only marks proliferative active liver cancer cells, while ATF4 protein not only can mark Ki67 positive cells, but also shows high expression in the whole liver tumor tissue compared with para-carcinoma tissue. In addition, the ATF4 protein is combined with other liver cancer biomarkers, so that cancer focuses can be positioned more accurately and comprehensively.

A preparation method and application of a double-regulated supramolecular assembly that inhibits tumor invasion and spread. Nano-supramolecular fiber aggregates constructed by supramolecular host-guest interactions. The advantages of the present invention are: the supramolecular assembly is oriented and aggregated under the induction of the geomagnetic field or a weak magnetic field, and can be light-controlled to induce the aggregation of the supramolecular assembly; on the other hand, the supramolecular assembly can specifically attract cancer cells, and the assembly can cause damage to mitochondria; the preparation method of the supramolecular assembly with dual regulation of magnetic field and light is simple, easy to implement and low in raw material cost, making it widely used in the field of tumor treatment, especially in Active inhibition of tumor cell invasion and spread has broad application prospects.

The invention provides an impedance sensing method for monitoring population cell invasion in a three-dimensional matrix. The method comprises the following steps: S1, preparing a conductive chip with a microelectrode array; s2, surrounding the periphery of the conductive chip with the annular structure to form a cell culture cavity; s3, performing surface treatment on the conductive chip; s4, fully paving cells on the microelectrode array of the cell culture cavity and forming polymeric hydrogel; s5, performing cell impedance detection in real time to obtain impedance information of the cells so as to obtain information of a cell invasion process. According to the invention, collagen I type gel suitable for a tumor invasion model is prepared on a microelectrode array conductive chip fully paved with cells through a self-assembly fibrosis process, and efficient and stable charge transfer in a cell impedance sensing detection process is effectively realized in combination with an impedance spectrometer on-line detection system; therefore, the technical effects of real-time, quantitative, label-free and whole-course dynamic analysis are achieved for detecting the invasion of the population cells in the three-dimensional matrix.

Disclosed herein is treating, reducing the incidence of one or more activities in or of cancer cells, or preventing one or more activities in or of cancer cells Methods of multiple activities, methods of treating, reducing the incidence of, or preventing migration or metastasis of cancer cells, by reducing tumor-associated macrophages (TAMs) or their migration Methods of treating cancer, reducing the incidence of cancer or preventing cancer, and treating cancer, including metastases, reducing the incidence of cancer, including metastases, for example using inhibitors of motile sperm domain-containing protein 2 (MOSPD2) or Methods of preventing cancer, including metastatic cancer. Also disclosed are inhibitors of MOSPD2 (eg, anti-MOSPD2 antibodies or antigen-binding fragments thereof) and pharmaceutical compositions containing MOSPD2 inhibitors. Also disclosed are methods for predicting, diagnosing, or prognosing cancer, cancer metastasis, tumor progression, or tumor invasion in a subject.

A recombinant fusion protein able to resist against tumor invasion and transfer is composed of the recombinant urokinase fragment and type-2 mutant as plasminogen activator inhibitor. The fusion protein gene cDNA is amplified by PCR method, and is cloned to expression vector to obtain fusion gene expression plasmid, which is used to transform host bacteria. The methanol or temp can induce the expression of said fusion protein. After purified, a high-purity (95%) expression product is obtained.

The invention discloses application of valproic acid in preparation of a multidrug resistance reversal agent of a lung cancer resistance medicine, and further discloses application of the valproic acid in the preparation of chemotherapeutics sensitizer of lung cancer resistance and a multidrug resistance tumor invasion resisting and transferring medicine. The application of the valproic acid in the preparation of the multidrug resistance reserval agent of the lung cancer resistance medicine verifies that valproic acid has significant function of a cisplatin persister of human lung cancer resistance through experiments, and verifies that the valproic acid can significantly change drug tolerance of a human lung cancer cell to the cisplatin, improve sensitivity of the human lung cancer cell to the cisplatin, and have obvious restraining effect of invasion effect of the persister of the lung cancer cisplatin.

Disclosed herein are methods of treating, reducing the incidence of, or preventing one or more activities in or of a cancer cell, methods of treating, reducing the incidence of, or preventing migration or metastasis of a cancer cell, methods of treating, reducing the incidence of, or preventing a cancer by reducing tumor associated macrophages (TAMs) or their migration, and methods of treating, reducing the incidence of, or preventing a cancer (including metastatic cancer), for example, with an inhibitor of Motile Sperm Domain containing Protein 2 (MOSPD2). Also disclosed are inhibitors of MOSPD2 (e.g., anti-MOSPD2 antibodies or antigen binding fragments thereof) and pharmaceutical compositions containing MOSPD2 inhibitors. Also disclosed are methods for the prediction, diagnosis, or prognosis of cancer, cancer metastasis, tumor progression, or tumor invasiveness in a subject.

The invention relates to an anti-tumor combined preparation and an application thereof. The preparation comprises a percutaneous immune membrane and an immune checkpoint blocking agent. According to the invention, the percutaneous tumor immune membrane is prepared mainly based on an alcohol plasma preparation technology and an electrostatic spraying technology, and an immune checkpoint blocker iscombined for antagonizing an immunosuppression pathway in T cells and enhancing CD8+ T cell mediated tumor destruction, so that long-term protection is provided, and tumor invasion, metastasis or recurrence is prevented.

The invention relates to a cholangiocarcinoma cell medicine target point. The medicine target point is ubiquitin specific protease 8, and the nucleotide sequence is shown as SEQID NO:1 in a sequence table. For the first time, the invention puts forward that USP8 is knocked down, so that proliferation, migration and invasion of cholangiocarcinoma cells can be notably restrained, MMP9 activity achieving important effects on cell adhesion, neoplasm invasiveness and transfer is reduced, and the USP8 is promoted to achieve effect of oncogene for growth and transfer ability of cholangiocarcinoma. New possibility is provided for development of cholangiocarcinoma medicines and cholangiocarcinoma prevention, treatment and prognosis.