412 results about "Glioma cell" patented technology

Peptides of influenza virus hemagglutinin protein and Plasmodium falciparum malaria antigen, antibodies specific for the peptides, influenza vaccines, malaria vaccines and methods of stimulating the immune response of a subject to produce antibodies to influenza virus or malaria are disclosed. Also disclosed are methods for formulating vaccines for influenza virus.

The invention discloses application of a crRNA mediated CRISPR / Cas13a gene editing system in tumor cells. According to the invention, in a U87 glioma cell system, a Cas13a protein can be mediated ontocomplementary target RNA by single-stranded crRNA and is cut. Meanwhile, the Cas13a protein can also trigger a joint shearing effect in eucaryotic cells, i.e., after starting to cut a first piece oftarget RNA, the Cas13a protein carries out aimless random cutting on other encountered RNA so as to take effects of inhibiting and killing tumors, such as effects of reducing a tumor cell index, inhibiting a mouse tumor formation rate and a tumor size. The invention provides a novel method for inhibiting or killing the tumor cells so as to lay a foundation for application of a random shearing effect of the CRISPR-Cas13 system in eukaryotic cells.

Compositions for use in characterization, diagnosis, prognosis, and therapy of cancer cells are provided. The compositions comprise peptides and variants thereof which were isolated based on their ability to selectively bind glioma cells.

The invention relates to a marine bacillus and its polypeptide with antitumor activity. The strain is preserved at China Center for Type Culture Collection in Wuhan, and its preservation number is CCTCC M 2013063. A novel marine bacillus polypeptide with anti-tumor activity is obtained from a fermentation product of the strain. By means of an MTT method, the invention finds that the polypeptide has an obvious proliferation inhibition effect on human hepatoma carcinoma cell BEL-7402, human breast cancer cell MCF-7, human glioma cell U251, human non-small-cell lung cancer cell A549 and other tumor cells, has relatively small cytotoxicity on human fibroblast HFL1, and can be applied in drugs treating human liver cancer, gliomas, lung cancer and breast cancer.

The invention belongs to the field of medicine preparation, and in particular to a targeting nanometer drug delivery system aiming at glioma, and a preparation method and application thereof. The drug delivery system comprises target functional molecules, a drug and nano carriers. The target functional molecules are from short chain polypeptide from interleukin 13; the drug is a micromolecular anti-glioma drug; the nano carriers are liposome with surface modified by polyethylene glycol, nanoparticles, polymeric vesicles, polymer micelles and solid lipid nanoparticles; and the drug is enveloped in the nano carriers in an enveloping or covalent connection manner, and the short chain polypeptide is connected with the polyethylene glycol on the surfaces of the nanoparticles through covalent connection. The drug delivery system can promote uptake of the glioma cells by mediated effect of an interleukin 13 receptor alpha 2 on the surfaces of the glioma cells, so as to improve the effect of anti-glioma chemotherapeutics.

The invention provides application of a compound shown in the formula (I) or a salt thereof in the aspects of preparing of medicines for treating malignant glioma or a mitochondrial targeting drug delivery system, and in the formula (I), R is C10-C18 alkyl, or R is benzyl. The experiments find that compared with a control, a berberine derivative not only can more effectively inhibit glioma cell proliferation, and can also effectively inhibit the migration and invasion ability of cells. In addition, the compounds can be well positioned to mitochondria, so that the compounds can be used as the mitochondrial targeting drug delivery system.

The invention relates to a method for preparing a dual-function targeting quantum dot lipidosome. The method comprises the following steps: preparing a single quantum dot lipidosome: dissolving phospholipid, cholesterol, methoxy polyethylene glycol-phospholipid complex and NRP-1 ligand polypeptide polyethylene glycol phospholipid complex into chloroform to obtain a uniform lipid membrane, and drying the chloroform by evaporation; dissolving in an ammonium sulfate solution of quantum dots, and oscillating to obtain lipidosome suspension; extruding, and diluting with normal saline to obtain an active targeting lipidosome containing the quantum dots; adding the active targeting lipidosome containing the quantum dots into an adriamycin normal saline solution, and treating in a water bath for 20 minutes at the temperature of 60 DEG C; and diluting with normal saline through a SephadexG-50 gel column, removing free medicaments, and thus obtaining the dual-function targeting quantum dot lipidosome. The lipidosome prepared by the method can be used for marking and treating glioma cells.

The invention discloses an antisense oligonucleotide which can inhibit the expression of human microRNA-133a and application thereof. The antisense oligonucleotide specificity is combined with the human miR-133a and contains the consecutive nucleotide sequences complementary with the following nucleotide sequence: 5'-UUUGGUCCCCUUCAACCAGCUG-3', especially 5'-CAGCUGGUUGAAGGGGACCAAA-3'. The antisense oligonucleotide can be used as the chimera of ribonucleotides or deoxyribonucleotides or ribonucleotide with deoxyribonucleotide and can modify any nucleotide in the chains. The miR-133a antisense oligonucleotide can effectively inhibit the miR-133a expression in human brain glioma cells, and can inhibit the growth and proliferation of human brain glioma cells, thereby effectively treating braingliomas and other tumors with high miR-133a expression.

The invention relates to interference small molecule ribose nucleic acid (RNA) of a targeted LIN28 gene and glioma migration resistant application thereof. The interference small molecule RNA is in a base sequence shown as SEQ NO.1. In the invention, the interference small molecule RNA of the gene with the effect of inhibiting glioma proliferation is provided, a glioma cell model is used for researching the inhibiting effect of the interference small molecule RNA on the glioma proliferation, and a new method is provided for genetic therapy of glioma.

A human chimeric antigen receptor targeting PDPN gene and its use, which contains a single-chain antibody hPDPNscFV against human PDPN antigen and a T cell stimulating signal transduction structure, wherein the light chain of the single-chain antibody hPDPNscFV can be The variable region and the heavy chain variable region are connected by a connecting peptide, the amino acid sequence of the connecting peptide is shown in SEQ ID NO.5, the scFV in the chimeric antigen receptor has the specificity of anti-human PDPN, and can specifically The chimeric antigen receptor can be used to modify T lymphocytes, and the modified T cells can be used for the treatment of PDPN-positive tumors, especially for surface tumors. PDPN-positive glioma cells have a specific killing effect.

The invention relates to applications of nicotinamide adenine dinucleotide in the field of pharmacy, and more specifically relates to applications of nicotinamide adenine dinucleotide in preparation of a medicine used for curing liver damages caused by chemotherapy drug doxorubicin hydrochloride. NAD<+> is capable of preventing and treating liver damages caused by chemotherapy drug doxorubicin hydrochloride effectively; and it is also found that NAD<+> is capable of killing glioma cells, neuronal tumor cells, gastric cancer cells, renal tumor cells or breast tumor cells effectively, but possesses no killing effect on normal primary cells.

The present invention demonstrates the therapeutic use of ketone esters for seizure disorders, Alzheimer's disease and malignant brain cancer, which are associated with metabolic dysregulation. The administration of ketone esters resulted therapeutic ketosis and neuroprotection against seizures resulting from CNS oxygen toxicity. Supplemental ketones were also found to reduce superoxide production in cultured cortex neurons exposed to hyperbaric oxygen and Aβ-42, and to decrease proliferation and viability in U87 glioma cells. These observations support the therapeutic effect of ketones for seizure disorders, Alzheimer's disease and malignant brain cancer. The ketone esters may be derived from acetoacetate and can include R,S-1,3-butanediol acetoacetate monoester, R,S-1,3-butanediol acetoacetate diester, or a combination of the two.

The invention discloses an antisense oligonucleotide for suppressing the expression of microRNA (ribose nucleic acid)-145 and application of the antisense oligonucleotide. The antisense oligonucleotide is specifically combined to human miR-145 and comprises a sequence complementary with at least thirteen continuous nucleotides in the nucleotide sequence of 5'-GUCCAGUUUUCCCAGGAAUCCCU-3', and particularly comprises the sequence of 5'-AGGGAUUCCUGGGAAAACUGGAC-3'. The antisense oligonucleotide can be a ribonucleotide, a deoxyribonucleotide or a chimera of the ribonucleotide with the deoxyribonucleotide, and an optional nucleotide in a chain can be modified. The miR-145 antisense oligonucleotide is capable of effectively suppressing the expression of miR-145 in human cerebral glioma cells, and suppressing growth and proliferation of the miR-145, thereby effectively treating cerebral gliomas and other miR-145 highly-expressed tumors.

The invention discloses a method for knocking out EGFRwt and EGFRvIII simultaneously from glioblastoma multiforme and relates to the recombinant DNA technology. The target site of sgRNA in an EGFR gene is on exon 17 of the EGFR gene, and is a gene sequence expressing a transmembrane region of the EGFR. According to the method for constructing Cas9 and sgRNA lentiviruses and infecting the glioblastoma multiforme with the lentiviruses, EGFRwt and EGFRvIII can be knocked out simultaneously from the glioblastoma multiforme. EGFRwt and EGFRvIII can be knocked out simultaneously and stably from the glioblastoma multiforme with the method, and occurrence and development of tumor can be inhibited effectively after knockout. The sgRNA is expected to be applied to novel drugs for treating EGFR amplification type and EGFRvIII mutant type glioblastoma multiforme.

The present invention relates to an RNAi molecule suitable for reducing the expression of galectin-1 containing any of the sequences of SEQ ID NOs: 1-33, and preferably the sequences of SEQ ID NO: 2, 3, or 4, and to the use thereof as a medicament, or for the manufacture of a medicament for treating and / or for delaying the progression of cancer, preferably glioma, pancreatic cancer, head and neck cancer, melanoma, non-small-cell lung cancer and non-Hodgkin's lymphoma. The present invention also relates to compositions and methods for treating and for delaying the progression of cancer, preferably glioma, pancreatic cancer, head and neck cancer, melanoma, non-small-cell lung cancer and non-Hodgkin's lymphoma, for reducing the migration of tumor cells, preferably cells of glioma, pancreatic cancer, head and neck cancer, melanoma, non-small-cell lung cancer and non-Hodgkin's lymphoma, and / or for enhancing the efficacy of cancer therapies for the treatment of cancer, preferably glioma, pancreatic cancer, head and neck cancer, melanoma, non-small-cell lung cancer and non-Hodgkin's lymphoma, selected from the group comprising chemotherapy, radiation therapy, immunotherapy, and / or gene therapy.

This invention relates to a method for constructing 9LLUC cell strain capable of stably expressing firefly luciferase PGL3. This invention provides a cell strain 9LLUC, which is obtained by transfecting glioma cell 9L with lentivirus vector containing firefly luciferase PGL3 gene, and screening. Cell strain 9LLUC can be transplanted into different animals to obtain relative glioma animal models. Though stable expression of PGL3, the generation, development, infiltration, metastasis of glioma cell, and the curative effects of relative therapies can be real time observed. The glioma animal models can be used for studying the development of glioma, and screening relative drugs and therapies.

The invention discloses micro-molecular interference ribonucleic acid (RNA) for inhibiting glioma proliferation and promoting glioma apoptosis as well as a preparation method and application thereof. The micro-molecular interference RNA has base sequences shown as SEQ ID NO.1 and SEQ ID NO.2. According to the invention, the micro-molecular interference RNA of a gene which has effects on inhibiting the glioma proliferation and promoting the glioma apoptosis is designed, a glioma cell model is utilized to research the effects of the micro-molecular interference RNA on inhibiting the glioma proliferation and the promoting glioma apoptosis, and a new method is provided for gene therapy of glioma.

The invention relates to novel beta-chloroethylnitrosourea compounds, and a synthesis method and application thereof. The structure of the beta-chloroethylnitrosourea compounds is disclosed as general formula (II). The in-vitro antitumor screening test on the compounds disclosed as general formula II proves that the compounds disclosed as general formula I have obvious inhibiting action on human cerebral nerve glioma cells SF763, SF767, SF126 and SF188, human colon cancer cell HT29, mouse leukaemia cell L1210 and many other tumor cell lines and have higher tumor inhibiting activity than the existing CENU and CENU / O6-benzylguanine combined medicine.

The instant invention has developed viral vectors encoding a mutant bacterial cytosine deaminase (bCD) gene, which have a higher affinity for cytosine than wild type bCD (bCDwt). The purpose of the present invention was to evaluate cytotoxicity in vitro and therapeutic efficacy in vivo of these vectors in combination with the prodrug 5-FC and ionizing radiation against human glioma. The present study demonstrates that infection with the viral vector expressing the mutant cytosine deaminase gene resulted in increased 5-FC-mediated cell killing, compared with vectors expressing the wild-type gene. Furthermore, a significant increase in cytotoxicity following infection with viral vector expressing the mutant cytosine deaminase gene and radiation treatment of glioma cells in vitro was demonstrated as compared to infection with viral vector expressing the wild-type gene. Animal studies showed significant inhibition of subcutaneous or intracranial tumor growth of D54MG glioma xenografts by the combination of AdbCD-D314A / 5-FC with ionizing radiation as compared with either agent alone, and with AdbCDwt / 5-FC plus radiation. These data indicate that combined treatment with this mutant enzyme / prodrug therapy and radiotherapy provides a promising approach for cancer therapy.

A diagnostic technique for matching anti-cancer peptide drugs to the molecular profiles of individual cancer tumors, and a method using the technique for a patient-specific treatment of tumors in mammals. This strategy matches anti-cancer peptide drugs to the molecular profiles of individual tumors, and includes the development of two banks, both of which use the same targeting peptides. Targeting peptides are identified using biopsies or other tissue materials from multiple cancer patients and placed into two banks. For a bank of probes, targeting peptides are linked to a label such as a fluorescent or a radioisotope. For a bank of drugs, targeting peptides are linked to a cytotoxic peptide to form a “targeting peptide drug”. Peptide probes are used to establish molecular profiles of individual tumors. Based on these molecular profiles, a patient-specific combination of targeting drugs from the bank of peptide drugs is prepared and the patient is treated. Any currently used cytotoxic agent that can be linked to targeting peptides may be used in place of cytotoxic peptides.

The invention belongs to the biological technical field, and relates to a targeting nano drug delivery system aiming at brain glioma modified by short peptides of a low density lipoprotein receptor, and a preparation method and application thereof. The drug delivery system comprises target functional molecules, a drug and nano carriers. The target functional molecules are from the short peptides of the low density lipoprotein receptor, obtained by phage display technology. The drug is enveloped in the nano carriers in an enveloping or covalent connection manner, and the short peptides are connected with the polyethylene glycol on the surfaces of the nanoparticles through covalent connection. The drug delivery system can invade and immerse tumor cells by hemato encephalic barrier, can enter into the tumor cells by EPR (enhanced permeability and retention effect), and can promote uptake of brain glioma cells by mediated effect of the low density lipoprotein receptor on the surfaces of the glioma cells so as to improve the effect of anti-brain glioma chemotherapeutics.

The invention relates to a marine natural anti-glioma active substance, and preparation and application thereof. The invention provides a Streptomyces filipinensis strain of which the classification designation is Streptomyces filipinensis ZQ-22. The Streptomyces filipinensis ZQ-22 is separated and cultured from soil under mangrove. The Streptomyces filipinensis is subjected to fermentation and extraction separation purification to obtain the anti-glioma active compound Bagremycin C. The compound obviously inhibits different glioma cells from proliferation, obviously induces the tumor cell apoptosis and influences the tumor cell period, and can be applied to preparation of drugs for treating glioma. The chemical structural formula of the Bagremycin C is disclosed in the specification.

The invention provides a recombinant adenovirus vector regulated by miRNA (micro Ribose Nucleic Acid) and capable of specifically proliferating in glioma cells. The recombinant adenovirus vector provided by the invention is characterized in that the target spot nucleotide sequence of at least one miRNA is inserted into the 3-untranslated region of at least one proliferation essential gene of the virus, the expression of miRNA is absent or reduced in glioma cells, but miRNA is normally expressed in nerve cells and glial cells so that the modified recombinant adenovirus specifically proliferate in the adenovirus in which the expression of miRNA is absent or reduced, but do not proliferate in normal cells in which the miRNA is normally expressed; and therefore, the recombinant adenovirus does not generate cytotoxicity to the normal cells.

The invention provides application of sinomenine to preparation of a medicament for treating human brain glioma. As proved by experiments, the sinomenine has a function of restraining human-derived glioma U87MG and SF767 cell strains, and the function is improved along with the increase of dose and time. Moreover, the sinomenine can induce the increase of autophagosomes, increase the quantity of autophagic vesicles, prompt the expression increase of human glioma cells LC3B-II, induce autophagic death of human glioma cells, and restrain the growth of U87MG cell xenograft tumors. The sinomenine is a novel and effective glioma-resisting medicament with a great potential, and can be used for preparing a human brain glioma medicament; by adopting the sinomenine, a new way is created for medical treatment of human brain glioma, and the medical application of the sinomenine is expanded.

This invention relates to compositions and methods utilizing a chemotherapeutic drug and 6-bromoindirubin3′-oxime (BIO) for the treatment of cancer, including glioblastoma multiforme. The present invention demonstrates that BIO works synergistically with chemotherapeutic drugs to increase the cytotoxic effects of these drugs in glioma cells.

The invention relates to the technical field of biological medicines, in particular to an application of a polypeptide in preparation of a drug for preventing and treating glioblastoma. The polypeptide has the functions of inhibiting cell proliferation of glioblastoma and delaying a growing process of glioblastoma, is peptide fragments (SEQ ID NO:1) (Sequence Identifier Number:1) of 138 amino acids and positioned at NO 234 to 371 amino acids in a cell interior domain of a human TROY protein sequence, has the functions of blocking the combination of a TROY accepter with a downstream signaling molecule RKIP (Phosphatidylethanolamine Binding Protein), reducing TROY mediated NF-kB activation, and inhibiting the cell multiplication of glioblastoma.

The present invention provides a new drug to treat malignant glioma, which is the most prevalent type of primary tumor of the central nervous system (CNS). The present invention indeed shows that the isolated NFL-TBS40-63 peptide is highly specific for glioma cells, in which it triggers apoptosis. It is therefore presented here for use in a method for treating malignant glioma. The present invention further relates to the use of the NFL-TBS40-63 peptide for detecting specifically glioma cells either in vivo, or in vitro, or for addressing chemical compounds to said tumor cells.

Disclosed are compounds that are effective for selectively killing cancer cells. Compounds have been demonstrated to be especially effective for killing glioma cells, while exhibiting low toxicity to normal cells.

The invention relates to a ruthenium complex, a ruthenium-RGD (arginine-glycine-aspartic acid) peptide conjugate and a preparation method and application thereof. The conjugate is obtained by couplingtwo parts including the ruthenium complex (RuM) and RGD peptide (RGDfK). A general formula of the ruthenium complex RuM is as follows: [Ru(dmp)2(X-COOH)](PF6)2, wherein X represents a ligand: 1,2-dimethyl-1H-imidazole[4,5-f][1,10]phenanthroline. The RGD peptide is a commercial reagent (RGDfK, Shanghai Qiangyao Biotechnology Company). The conjugate RuM-RGD is obtained by taking the ruthenium complex RuM and the RGD peptide RGDfK and carrying out condensation reaction. The RuM-RGD conjugate provided by the invention has a strong inhibition effect on glioma cells U87, and can be used for accumulating mitochondria of the U87 tumor cells and inhibiting tumor cell proliferation; the RuM-RGD conjugate can be used as a novel anti-tumor medicine taking a tumor cell mitochondrion as a target spot.

The invention discloses a compound lithocarolsA-F, a preparation method and application thereof in preparation of antitumor drugs. The compound lithocarolsA-F is isolated from a fermentation culture of marine fungi Phomopsis lithocarpus FS508. Experiments prove that the IC50 values of the compound lithocarolsA-F on liver cancer cells HepG-2, breast cancer cells MCF-7, glioma cells SF-268 and non-small cell lung cancer cells A549 are 10.5-87.7 muM, showing that the compound lithocarolsA-F has relatively significant antitumor activity and can be used for preparing antitumor drugs.