51 results about "U87" patented technology

The invention discloses an antisense oligonucleotide used for inhibiting the expression of micro RNA-485-5p, and an application thereof. The antisense oligonucleotide comprises the sequence of 5'-GAAUUCAUCACGGCCAGCCUCU-3' which can be specifically combined with human miR-485-5p. The antisense oligonucleotide can be ribonucleotide, deoxyribonucleotide or chimera of the ribonucleotide and the deoxyribonucleotide, and can be used for modifying any nucleotide in the chain. The miR-485-5p antisense oligonucleotide can be used for effectively inhibiting the expression of miR-485-5p in a human brainglioma cell U87 as well as the growth and propagation of the human brain glioma cell U87, thus effectively treating the brain glioma and other tumours with high expression of miR-485-5p.

The invention discloses a nucleic acid aptamer specifically bound with a human epidermal growth factor receptor III-type mutant and an application of the nucleic acid aptamer. The nucleotide sequence of the nucleic acid aptamer is any one of SEQ ID NO:1, SEQ ID NO:2, SEQ ID NO:3 and SEQ ID NO:4. The nucleic acid aptamer specifically bound with the human epidermal growth factor receptor (EGFRv) III-type mutant is only specifically bound with U87-delta cell lines rather than U87 cell lines, so that the nucleic acid aptamer can be effectively applied to preparing a sensor or a kit for diagnosing tumor cells for expressing EGFRv III. Furthermore, the nucleic acid aptamer can be adopted as a medicine carrying tumor cells resistant to express EGFRv III or a carrier of siRNA (Small Interfering RNA) for entering tumor cells or tissues capable of expressing EGFRv III so as to play a role of a targeted matter, thereby having broad application prospects.

The invention discloses antisense oligonucleotide for suppressing the expression of micro ribonucleic acid (RNA)-150 and application thereof. The antisense oligonucleotide comprises a sequence, namely, 5'-CACUGGUACAAGGGUUGGGAGA-3', wherein the sequence can be specifically combined with human miR-150. The antisense oligonucleotide can be ribonucleotide, deoxyribonucleotide or the chimera of the ribonucleotide and the deoxyribonucleotide and can modify any nucleotide in a chain. MiR-150 antisense oligonucleotide can effectively suppress the expression of miR-150 in a human glioma cell U87, suppresses the growth and multiplication of the cell and can effectively treat brain glioma and other tumors with high miR-150 expression.

The invention provides application of compound of any one or more of a formula I, a formula II and a formula III for the preparation of a medicament for treating brain malignant gliomas or melanoma and belongs to the technical field of tumor medicines. The compound shown in the formula I, the formula II and the formula III is a monomer ingredient in an annona squamosa total lactones extract. The invention further provides a method for preparing an annona squamosa seed extract for treating human brain malignant gliomas or melanoma and a product thereof. The compound shown in the formula I, theformula II and the formula III and the extract (including effective parts) have an efficient killing effect on the brain malignant gliomas or melanoma. Particularly, the compound shown in the formulaI has an IC 50 value of only 0.4044 nM for brain malignant gliomas U87-MG, and an IC50 value of only 0.5152 nM for melanoma SK-MEL-28, while the IC50 for most other tumors is often between 1uM and 100uM, and the difference is more than three orders of magnitude, showing a selective and efficient killing effect on brain malignant gliomas U87-MG and melanoma SK-MEL-28.

The invention discloses a research method of a Crosstalk mechanism of VEGF-CXCL8-Akt and application thereof. The research method comprises the following steps of firstly, detecting the influence of U87MG, U251 and secretion factors VEGF thereof on secretion of CXCL8 by HBMEC by using ELISA, secondly, respectively adding a specific agonist CXCL8 and an inhibitor LY294002 of a CXCL8-Akt signal pathinto a co-culture system, and detecting the influence of co-culture and activation / inhibition on expression of Akt proteins of U87MG and U251 cells and phosphorylation activation state P-Akt thereofby using Western blotting, and then using CCK-8 and Transwell invasion experiments for respectively detecting the influence of co-culture and activation / inhibition on proliferation and invasion of U87MG and U251 cells.

The invention discloses a 3,5-disubsitutued 2-amino-pyrazine compound. The compound has the structure shown in the formula I; in the formula I, NR1R2 is n-propylamino, cyclopropylamino, cyclopentylamino, cyclohexylamino, morpholinyl, 4-methyl piperazine, anilino, 4-chloroaniline or 3-chloroaniline; Ar is 3,5-dimethyl-isoxazolyl-4 or 1-methyl-1H-pyrazolyl-4; and the invention further provides the preparation technology and application thereof. The compound has the outstanding inhibiting effect on growth of four kinds of cancer cells including a human cervical cancer cell HeLa, a human brain glioma cell U87, a human hepatoma cancer cell HepG2 and a human colon cancer cell LoVo, wherein a large part of the compound has an obviously higher inhibiting effect on proliferation of the cancer cellsthan positive control VX-680, particularly the compound Ih and Ii have relatively high activity on the four kinds of cancer cells, and have prominent activity inhibiting effect on aurora kinase A andaurora kinase B, and therefore the compound can be applied to preparation of anti-cancer drugs.

The invention provides a triterpenoid saponins compound, the molecular formula of which is C52H84O20 and the chemical name of which is 3b-O-[b-D-xylopyranose-(1-3)-a-L-rhamnopyranosyl-(1-2)-[b-D-glucopyranesyl-(1-4)]-a-L-arabopyranose] oleanolic acid (3b-O-[b-D-xylopyranosyl-(1-3)-a-L-rhamnopyranosyl-(1-2)-[b-D-glucopyranosyl-(1-4)]-a-L-arabinopyranosyl]oleanolicacid). An in-vitro antitumor test proves that the triterpenoid saponins compound has obvious inhibitory action on C6 rat spongioblastoma cell and four spongioblastoma cells: U87MG, U251MG, BT325 and SHG44, but has no influence on the growth of primarily cultured human neurogliocyte. The triterpenoid saponins compound can be used for preparing medicaments for treating glioma.

The invention discloses an application of low-temperature plasma combined with metformin, in particular the application of low-temperature plasma combined with metformin to non-therapeutically induce glioma cell death in vitro. The application of the combination of low-temperature plasma and metformin in in vitro non-therapeutic induction of glioma cell death provided by the present invention shows that the combination of low-temperature plasma and metformin has obvious effects on glioma cell lines U251 and U87 cells cultured in vitro Synergistic inhibitory effect, can significantly induce cell death. The present invention is used for non-disease treatment, but for in vitro research. The scheme of the application of the combination of metformin and low-temperature plasma in inducing the death of glioma provided by the present invention can be used to study the combination of low-temperature plasma and metformin in glioma. It provides a new strategy for the application of glioma treatment, in order to provide new ideas for the design of new products or new programs for the treatment of glioma.

The invention provides a bionic nanocarrier for treating GBM (glioblastoma) and a preparation method of the bionic nanocarrier and belongs to the field of biomedical engineering. According to the bionic nanocarrier for treating the GBM and the preparation method of the bionic nanocarrier, Ang-RBCm-CA / siRNA comprises Ang-RBCm (Ang (Angiopep-2) polypeptide modified red blood cell membrane) and citraconic anhydride grafted polylysine and polyethylenimine-siRNA compound (CA / siRNA). Ang-RBCm-CA / siRNA can effectively carry siRNA and protect siRNA against degradation. The Ang-RBCm-CA / siRNA has prolonged blood circulation time and high blood brain barrier penetrability, can be efficiently taken in by U87MG brain glial cells over-expressed by a low-density LPR (lipoprotein receptor) and can realizerapid charge conversion in endosome / lysosome, effectively release siRNA and effectively treat in-situ U87MG GBM.

The present invention provides an adeno-associated virus recombinant vector for knocking out the CXCL12 gene, the recombinant vector at least includes the following sequence elements operably linked: 5' terminal inverted repeat sequence, CMV promoter, sacas9 sequence, polyA signal sequence, U6 promoter sequence, gRNA sequence, 3'-end inverted repeat sequence. The inventors found that the CXCL12 gene knockout vector can effectively inhibit the growth of transplanted tumors and tumor angiogenesis in the U87 cell glioma model, and can effectively inhibit the tumor growth and tumor angiogenesis in the U87 cell subcutaneous glioma model in nude mice. It shows that the technical scheme of the present invention can be applied to the treatment of glioma diseases.

The invention discloses the application of a crRNA-mediated CRISPR / Cas13a gene editing system in tumor cells. In the U87 glioma cell line, the Cas13a protein of the present invention can be mediated by a single-stranded crRNA to a complementary target RNA and cut. At the same time, Cas13a protein can also trigger the effect of joint shearing in eukaryotic cells, that is, after starting to cut the first entry of RNA, Cas13a protein will randomly cut other RNAs encountered without purpose, thereby reducing Tumor cell index, inhibition of tumor formation rate and tumor size in mice and other effects of inhibiting and killing tumors. The invention provides a new method for inhibiting or killing tumor cells, and lays the foundation for the application of the random shearing effect of the CRISPR-Cas13 system in eukaryotic cells.

The invention provides application of miR-6858 in preventing and treating glioma through melatonin and belongs to the technical field of biomedicines. Specifically, the invention finds that melatoninhas a good antitumor function on cells U251, U87, A172 and GBM#P3. Meanwhile, through miRNA (micro ribonucleic acid) sequencing on GBM (glioblastoma multiforme) cells treated by using melatonin, target miRNA is found, growth of the GBM cells can be inhibited by increasing miR-6858 through the melatonin, and furthermore, an SIRT3 / AKT signal channel can be inhibited. The invention illuminates molecule mechanisms based on interactions melatonin and miRNA, and an effective treatment strategy is provided for treatment on GBM.

The invention discloses a novel spxiterpenoid saponin type compound extracted from Ardisia pusilla and the application thereof in treating glioma. A chemical structure of the compound is determined by adopting such spectroscopic technologies as high-resolution mass spectrum and two-dimensional nuclear magnetic resonance spectroscopy and the like as well as a chemical method. An in vitro anti-tumor experiment shows that the compound has remarkable effect on inhibiting four human malignant glioma cells comprising U87MG, U251MG, BT325 and SHG44 without affecting the growth of the primary cultured human neuroglial cells. The novel spxiterpenoid saponin type compound is expected to be a drug for curing glioma.