18 results about "U87" patented technology

The invention relates to the field of natural products, in particular to a dimer compound of guaiane type sesquiterpenes and uric acid as well as an extraction and separation method and application of the dimer compound. According to the invention, a new dimer compound of guaiane type sesquiterpene and uric acid is extracted and separated from carpesium abrotanoides in Guizhou, and it is found that the dimer compound has relatively strong anti-tumor activity. The compound has strong inhibitory activity on breast cancer, prostate cancer, nasopharynx cancer, liver cancer, lung cancer, leukemia, pancreatic cancer, glioma, osteosarcoma, skin cancer, cervical cancer, ovarian cancer, kidney cancer and esophageal cancer, and provides an optional scheme for broad-spectrum anti-cancer drugs. Moreover, in human prostate cancer cells PC3, human cervical cancer cells Hela, human liver cancer cells HepG2 and human glioma cells U87 which are resistant to paclitaxel, the compound also shows strong anti-cancer activity, which indicates that the compound has the potential of treating patients resistant to paclitaxel.

Through extensive and deep research, a new path Parkin / Park / Mul1 / Mfn2 for regulating and controlling the drug resistance of a tumor chemotherapy temozolomide (TMZ) drug by the TRPC5 is found, and the new path has a close relationship with the generation of the drug resistance of the tumor chemotherapy temozolomide (TMZ) drug. Compared with primary cells U87 and U251, the expression level of the TRPC5 in temozolomide tolerant cells U87R and U251R is remarkably improved, and a mitochondrial autophagy pathway is activated. By reducing the expression of the TRPC5 gene, the sensitivity of a cell strain to a temozolomide drug can be enhanced, and the proliferation capacity of tumor cells can be inhibited. According to the invention, not only is new data provided for a malignant glioma drug resistance mechanism, but also a new target spot is provided for the design of anti-tumor drug resistance drugs.

The invention discloses a drug delivery system containing loaded adriamycin as well as a preparation method and application of the drug delivery system. The drug delivery system comprises poly (beta-amino ester) coupled with adriamycin, wherein the surface of the poly (beta-amino ester) is coated with dextran sulfate, and the poly (beta-amino ester) takes a fourth-generation lysine dendritic molecule Lys-G4 as a core. The drug delivery system has a pH-dependent drug release characteristic, has remarkable toxicity to C6 and U87MG glioma cells, has the capabilities of inducing apoptosis, inhibiting migration and targeting subcellular localization, and can effectively penetrate through a blood-brain barrier model and 3D tumor spheres. The delivery system is compounded with PLA-PEG-PLA thermosensitive hydrogel, and the thermosensitive hydrogel with a drug storage function is successfully constructed. Good tumor inhibition effect and biocompatibility are shown in nude mouse subcutaneous and in-situ glioma models. The invention not only provides a new strategy for overcoming the blood brain barrier, but also can effectively reduce the systemic toxicity, and opens up a new research thought and method for glioma treatment.

The present application belongs to the technical field of biological medicine, and particularly relates to Hermetia illucens extract, an extraction method thereof and application thereof in preventing and treating tumors. The present application extracts polar components from Hermetia illucens powder, and the obtained Hermetia illucens extract has a significantly better inhibitory activity on the proliferation of Cal27 human tongue squamous cell carcinoma cells, Colo205 human colorectal cancer cells and U87 MG human brain astrocytoma cells than the Hermetia illucens powder without separation under the same mass concentration. In animal experiments, the Hermetia illucens extract can significantly prolong the survival cycle of MOC-1 tongue squamous cell carcinoma mice, and has a significantly better treatment effect than the Hermetia illucens powder and is close to the positive drug cisplatin.

The application discloses the application of Huaxingdan in the preparation of a glioma drug in the technical field of biology and medicine, detects the influence of Huaxingdan on the proliferation activity of glioma cells U251, U87 and A172 by using an MTT method in vitro, finds that Huaxingdan has a significant inhibitory effect on the proliferation of glioma cells, and is time and concentration dependent. The influence of Huaxingdan on the apoptosis of glioma cells U87 is detected by using a flow cytometry, and it is found that Huaxingdan can induce the apoptosis of U87 cells, and is concentration dependent. The animal experiment shows that Huaxingdan can effectively inhibit the growth of glioma cells in vivo, and the HE staining shows that Huaxingdan has no toxicity in vivo, and can be used as a drug for preventing and treating glioma.

This invention relates to a biomimetic nanodelivery system ANG-2-CMLNPs. The preparation method of ANG-2-CMLNPs includes the following steps: Step 1: Prepare EZ NPs using a one-step self-assembly method, then co-incubate them with siRNA to obtain siRNA-EZ NPs; Step 2: Prepare liposomes using a thin-film hydration method, then modify them with ANG-2; Step 3: Add U87 MG cells to cold PBS, centrifuge to remove intact cells and debris, and the resulting precipitate is the glioma cell membrane fusion membrane; Step 4: Mix the Angiopep-2 modified liposomes obtained in Step 2 with the glioma cell membrane fusion membrane obtained in Step 3, and sonicate to obtain a composite; Step 5: Co-extrude the composite obtained in Step 4 with the siRNA-EZ NPs obtained in Step 1 to obtain the biomimetic nanodelivery system ANG-2-CMLNPs; In the above preparation process, when EZ... When the mass ratio of NPs to siRNA is 125:1 and the mass ratio of ANG-2 modified liposomes to CM is 1:5, the prepared ANG-2-CMLNPs delivery system achieves the optimal functional balance between the ability to cross the blood-brain barrier (BBB) ​​and tumor targeting efficacy.

The invention relates to the technical field of biomedicine, in particular to a novel target spot for resisting chikungunya virus infection and application. According to the invention, human neuroblastoma cells (SH-SY5Y) and human brain astroblastoma cells (U87) are taken as target cells, and the expression of the target cell part capable of exerting receptor action membrane protein is down-regulated by adopting an RNA interference technology, so that a host factor capable of effectively inhibiting CHIKV infection of human nerve cells is found, and the purpose of blocking CHIKV infection from the source is achieved. It is found that platelet membrane glycoprotein VI (GP6) plays an important role in CHIKV infection SH-SY5Y and U87 cells, expression of GP6 is reduced, and CHIKV infection can be obviously inhibited. The invention provides an application of GP6 in preparation of a medicine for preventing or treating chikungunya virus infection, and provides a new target spot and a treatment scheme for clinically preventing and treating fever, arthralgia, joint swelling, muscle pain, headache, nausea, fatigue, rash and other diseases caused by CHIKV infection.

The application relates to the technical field of biological medicine, and discloses application of Nilotinib in preparation of a drug for inhibiting p53-AKT interaction. Relying on a double-fluorescence reporting system NanoBRET system, high-throughput screening is completed at a live cell level, and it is determined that a tyrosine kinase inhibitor Nilotinib can inhibit p53-AKT interaction. Function verification shows that Nilotinib can dose-dependently destroy a p53-AKT complex in HEK293T tool cells and U87MG, T98G and other glioma cells, release the inhibition of p53 function, and induce cell apoptosis. The above results illustrate a new path of precise intervention with the "p53-AKT interface" as a target, and provide experimental basis for redirecting Nilotinib to overcome p53-related drug resistance.

This invention discloses a method for verifying TBCB glioblastoma and cell proliferation, belonging to the fields of bioinformatics and tumor molecular biology. S1: Constructing a TBCB knockdown model and verifying its effectiveness; S2: Obtaining transcriptome data from the knockdown group and control group using RNA-seq; S3: Obtaining a set of DEGs through differential expression analysis; S4: Performing disease enrichment analysis based on DisGeNET to obtain significantly enriched disease entries and screening for GBM / glioma-related entries; S5: Verifying the expression differences and clinical relevance of TBCB and GBM based on public databases (one or more of GEO / TCGA / CGGA); S6: Conducting an EdU incorporation experiment in U87 cells to quantitatively verify the effect of TBCB knockdown on cell proliferation. The verification method of this invention is more directly disease-targeting: by using DisGeNET disease enrichment, the DEGs set is directly mapped to specific disease entries such as "glioma / glioma," avoiding a focus solely on pathway levels.

The application discloses a preparation method and application of a novel dimeric RGD cyclic peptide nuclear medicine targeting integrin alpha v beta 3, relates to the fields of radiochemistry and biological medicine, and discloses a preparation method and application of a nuclide marker targeting alpha v beta 3 integrin. The alpha v beta 3 nuclear medicine designed and synthesized in the application has good in-vivo stability, pharmacokinetic properties, and strong targeting and uptake to U87MG tumor cells with high expression of alpha v beta 3, and has diagnosis or treatment properties, and is expected to become a nuclide nuclear medicine with good application prospect for targeting alpha v beta 3 induced tumors.

The invention belongs to the technical field of polypeptide drugs, and particularly relates to a series of polypeptides with an anti-cancer effect and application thereof. According to the invention, Rink amide MBHA amino resin is used as a solid phase carrier, modification is carried out according to an amino acid sequence of a template polypeptide Hymenochirin-1Pa (H-0): Ac-LKLSPKTKDTLKKVLKGAIKGAIAIASAMA-NH2, and on the basis of retaining key amino acid residues, original amino acids are replaced by R8 and S5 at the positions of i and i + 7 amino acids, so that the target stapling peptide is obtained. Compared with a template polypeptide H-0, the obtained stapled peptide has the advantage that the anti-tumor activity on human liver cancer cells Huh7, human non-small cell lung cancer cells A549, glioma cells U87 and colon cancer cells T84 can be obviously improved.

The application discloses a cell-penetrating peptide modified enzyme-sensitive PDC type PROTAC as well as a preparation method and application thereof, and belongs to the technical field of tumor targeted therapy. The cell-penetrating peptide modified enzyme-sensitive PDC type PROTAC is obtained by modifying a cell-penetrating peptide and an enzyme-sensitive linker (GFLG) to a PROTAC of an anti-tumor drug target protein ligand, has the ability to release the PDC type PROTAC under catalysis of cathepsin B, has a smaller influence on cell viability of U251 cells, U87 cells and HEK293 cells, has proliferation inhibition activity on the U251 cells and the U87 cells, can degrade target proteins in the U251 cells and the U87 cells, can induce apoptosis of the U251 cells and the U87 cells, has an influence on U251 cell cycles, can be used for preparing an anti-tumor drug (target protein degradation and membrane penetration), has a good application prospect in preparation of a drug for targeting human brain glioma cells, and can be used as another important field for PROTAC drug development.

The invention relates to the technical field of biomedicine, in particular to a novel target spot for resisting chikungunya virus infection and application. According to the invention, human neuroblastoma cells (SH-SY5Y) and human brain astroblastoma cells (U87) are taken as target cells, and the expression of the target cell part capable of exerting receptor action membrane protein is down-regulated by adopting an RNA interference technology, so that a host factor capable of effectively inhibiting CHIKV infection of human nerve cells is found, and the purpose of blocking CHIKV infection from the source is achieved. The invention discovers that the nerve cilia protein 2 (NRP2) plays an important role in CHIKV infection SH-SY5Y and U87 cells, and the CHIKV infection can be obviously inhibited by down-regulating the expression of the NRP2. The invention provides an application of NRP2 in preparation of a medicine for preventing or treating chikungunya virus infection, and provides a new target spot and a treatment scheme for clinically preventing and treating fever, arthralgia, arthrocele, muscular pain, headache, nausea, fatigue, rash and other diseases caused by CHIKV infection.

The present application relates to the field of natural products, in particular to a sesquiterpene and uric acid dimer compound of guaiane type and an extraction and separation method and application thereof. A new sesquiterpene and uric acid dimer compound of guaiane type is extracted and separated from Guizhoutianmingjing, and it is found that the compound has strong antitumor activity. The compound has strong inhibitory activity on breast cancer, prostate cancer, nasopharyngeal carcinoma, liver cancer, lung cancer, leukemia, pancreatic cancer, glioma, osteosarcoma, skin cancer, cervical cancer, ovarian cancer, kidney cancer and esophageal cancer, and provides an alternative for broad-spectrum anticancer drugs. Moreover, in the paclitaxel-resistant human prostate cancer cell PC3, human cervical cancer cell Hela, human hepatoma cell HepG2 and human glioma cell U87, the compound also exhibits strong anticancer activity, indicating that it has the potential to treat paclitaxel-resistant patients.

This invention relates to the field of genetic engineering technology, disclosing a method for constructing a plasmid for knocking out the FOSB gene, the plasmid constructed by the above method, and the application of the plasmid in preparing transfection reagents for knocking out the FOSB gene in cell lines; it also discloses a FOSB gene knockout method based on the CRISPR-Cas9 system, FOSB gene knockout cells, and their applications. This invention provides a method for designing dual sgRNAs targeting exons 2 and 3 of the FOSB gene, overcoming technical bottlenecks such as polyploidy / alloidy in U87-MG cells, high DNA repair capacity, and easy phenotype recovery, significantly improving knockout efficiency, causing frameshift mutations, resulting in complete loss of FOSB protein function, and constructing a knockout vector based on the PX459 plasmid, adapted to U87-MG cells, solving the problem of low conventional transfection efficiency; and successfully constructing the FOSB gene knockout vector. ∆ / ∆ The U87 cell line can be stably passaged for a long time, has a stable genetic background, and does not lose the knockout phenotype, providing a standardized and reproducible experimental platform for FOSB gene function research and glioma mechanism exploration.

The invention discloses an experimental method for researching TRPC5 for promoting glioma TMZ drug resistance by regulating MUL1 induced mitochondrial autophagy. The experimental method comprises the following steps: step 1, analyzing the change of the expression quantity of TRPC5 in recurrent glioma and primary glioma after TMZ chemotherapy; a TMZ-resistant U87 cell strain is constructed, and the change of the expression quantity of TRPC5 in TMZ-resistant U87 and normal U87 cells is analyzed, so that the relationship between TPRC5 and glioma TMZ drug resistance is determined. 2, analyzing the influence of exogenous overexpression TRPC5 on U87 glioma cell proliferation, invasion ability and TMZ drug resistance, constructing a nude mouse glioma intracerebral model, and verifying whether the nude mouse glioma intracerebral model has the same conclusion in the in-vivo environment; and exploring the expression of drug resistance of TMZ in brain glioma under other pathways / paths.

This invention discloses a naphthidone compound, its pharmaceutical composition, and its uses. The compound of this invention can effectively degrade the BRD8 protein in LNCAP cells and U87 cells, and exhibits certain anti-proliferative activity against LNCAP cells. Therefore, the above compound can be used to prepare drugs for the prevention and / or treatment of diseases related to the BRD8 protein, such as drugs for the prevention and / or treatment of glioblastoma, prostate cancer, etc.

The invention provides a CAR (Chimeric Antigen Receptor)-NK (Natural Killer) cell of glioma. The CAR-NK cell is prepared by the following steps: constructing a pMFG-EGFRvIII-CAR plasmid vector, preparing an anti-EGFRvIII-CAR retroviral vector, and preparing an anti-EGFRvIII-CAR-NK cell. The EGFRvIII-CAR-NK cell has strong killing activity to the U87-EGFRvIII cell, and the killing activity is obviously higher than that of the NK cell, so that the EGFRvIII-CAR-NK is proved to enhance the targeting capability and the killing activity of the EGFRvIII-CAR-NK cell.