34 results about "Glioma cell lines" patented technology

The invention provides a human brain glioma cell line and an establishing method and application thereof. The human brain glioma cell line is preserved in China Center for Typical Culture Collection with an accession number of CCTCC No. C201115. The human brain glioma cell line is established by subjecting brain glioma cells originated from a clinic specimen to primary culture and subculture, can be directly used for in vitro drug screening or generation of human brain glioma in mammals and is used for establishing a human brain glioma animal model and screening candidate drugs used for treating human brain glioma. The human brain glioma cell line has stable properties, can realize stable multiple passages and maintain stable properties even after in vitro passage to the 50th generation; pathogenesis of human brain glioma, drug susceptibility, transitivity and other related characteristics can be analyzed in vitro and in vivo, so two correlated in-vitro and in-vivo anti-brain glioma drug screening platforms can be established, and novel experimental materials closer to clinic oncobiological characteristics are provided for research on human brain glioma.

The invention discloses a semen lepidii anti-tumor effective component, a preparation method of the semen lepidii anti-tumor effective component and an application of the semen lepidii anti-tumor effective component in the field of anti-tumor. The preparation method comprises the following steps of: extracting semen lepidii (roasted) with water; and extracting with ethyl acetate and water saturated n-butyl alcohol sequentially; collecting water saturated n-butyl alcohol extract; separating with a silica (200 to 300 meshes) column; and performing gradient elution with dichloromethane-methanol in different proportions, wherein the dichloromethane-methanol (5:1) elution part is a semen lepidii anti-tumor effective part. The part has a remarkable effect of inhibiting U251 (glioma cell line), HepG2 (human hepatoma cell line), SGC (human gastric carcinoma cell), mcf-7 (human breast cancer cell) and SCLC (lung carcinoma cell), and can be used for preparing an anti-tumor medicament.

The present invention provides a TOP2A inhibition by temozolomide useful for predicting glioblastoma patient's survival. Glioblastoma (GBM) is the most common, malignant primary adult brain tumor. The conventional treatments for GBM, include surgery, radiation, and chemotherapy which have only modestly improved patient survival. The patients with GBM expressing higher TOP2A transcript levels had better prognosis. More interestingly, the present invention reports that temozolomide is an inhibitor of TOP2A activity in vitro. The present invention further shows that siRNA knock down of TOP2A rendered a glioma cell line resistant to temozolomide chemotherapy.; Thus it is demonstrated for the first time that temozolomide is a TOP2A inhibitor and establishes that TOP2A transcript levels determines the chemosensitivity of glioblastoma to temozolomide therapy thus explaining the very high levels of TOP2A transcript being a good prognostic indicator in GBM patients receiving temozolomide chemotherapy.

The invention relates to a glioma cell line. The glioma cell line is glioma cells infected by a virus vector. The virus vector comprises ITR (inverted terminal repeat), a promoter, a photosensitive gene, a green fluorescence labeling gene and ITR, which are sequentially connected. The glioma cell line is specifically marked by the light-sensing gene, and can generate stable light current under induction and stimulation of light, so that the glioma cell line can be selectively performed with specific regulation with light. The invention further provides a construction method of the glioma cell line.

The present invention relates the application of a human source dcf1 gene in the inhibition of U251 glioma cell line proliferation and in the induction of U251 glioma cell line apoptosis. The present invention makes judgments for dcf1-induced U251 cell line apoptosis by the methods of immune electron microscope, atomic force microscope, CCK8 proliferation detection, JC-1 staining, and nude mouce tumor heterotopic transplantation. The results show that: the dcf1 causes mitochondrial structure lesion and membrane potential reduction by locating in mitochondria, thereby causing apoptosis-related gene expression change, and eventually leading to apoptosis. The nude mouce experiments show that the dcf1 can significantly reduce glioma tumor volume and inhibit tumor growth.

The invention provides an application of a SHP-2 inhibitor in preparing a medicament for targeting preneuronal glioma. The invention also provides a medicament for treating the preneuronal glioma, which is a preparation prepared by using the SHP-2 inhibitor as an active ingredient and adding pharmaceutically acceptable auxiliary materials or auxiliary ingredients. The experimental results show that the SHP-2 inhibitor (SHP099) has little toxicity to normal cells, and the inhibitory effect on proliferation and clone formation of proneuronal glioma cell line is significantly stronger than that of a control cell line. SHP099 can also specifically induce cell cycle arrest in proneuronal glioma cell lines. Therefore, when SHP099 is used for inducing cell cycle arrest, TMZ or radiotherapy can becombined to further enhance the therapeutic reactivity of the proneuronal glioma. SHP099 has high blood brain barrier permeability after oral administration, so that the SHP099 has the best drug-forming property which is difficult to achieve by common SHP-2 inhibitors. The invention provides a novel treatment strategy of SHP099 specifically targeting the proneuronal glioma, and has good clinicalapplication prospect.

The invention discloses a new application of isojacareubin. The new application is meant that isojacareubin as an active ingredient is used in preparation of an antitumor pharmaceutical preparation. Pharmacological tests prove that, isojacareubin has an obvious inhibition effect on growth of U87 human brain glioma cell lines, BXPC-3 human pancreatic cancer cell lines, NCI-2126 human lung cancer cell lines, PANC-1 human pancreatic cancer cell lines, A549 human non small cell lung cancer cell lines, AGs human gastric cancer cell lines, A375 human melanoma cell lines, MCF-7 human breast cancer cell lines, MDA-MB-231 human breast cancer cell lines and SMMC-7721 human liver cancer cell lines, has significant antitumor activity, can be expected to be used as the active ingredient for the preparation of the antitumor pharmaceutical preparation, and has medicinal prospects.

The invention discloses an experimental method of MiR-210 in the verification of relevant targets in glioma. The experimental method is characterized by comprising the following steps of: using a glioma cell line, respectively constructing a miR-210 overexpression cell group, a miR-210 low-expression cell group and an empty granulocyte group, detecting the effect of miR-210 on the downstream genethrough the real-time qPCR, western blotting experiment, and detecting the expression level of the target protein and gene. The relevant biological effects of miR-210 are determined by MTT, invasion and migration. And whether the targets are correct by the reporter gene is determined.

The invention discloses a composition for inhibiting glioma growth and an application thereof. The composition comprises a substance for improving the expression of protein (PTEN) as shown in sequence 1 of the sequence table, and a substance for inhibiting the expression of protein (B) as shown in sequence 3 of the sequence table. Experiments demonstrate that when the combination of recovering the expression of protein PTEN with inhibiting the expression of protein B is compared with only recovery of the expression of protein PTEN or only inhibition of expression of protein B, the AKT phosphorylation level of recombinant glioma cell lines is significantly decreased, cell proliferation and colony formation are significantly inhibited, and the proportion of cells stopping at the G0 / G1 phase and the cell apoptosis rate are significantly increased; Glioma in transplanted mouse body has no increase in size at 20-48 days after treatment by recovering the expression of protein PTEN combined with inhibiting the expression of protein B, and the tumor weight is almost zero at the 48th day after the treatment. The invention provides a new and effective combination therapy scheme for glioma, and has wide application prospects.

The invention discloses an application of IncRNA LNC_004208 and detection reagent thereof in preparing a glioma prognosis reagent. Through research on and utilization of IncRNA sequencing, the invention finds that IncRNA LNC_004208 has ultrahigh expression in a temozolomide-resisted glioma cell line; through telephone follow-up for 104 glioma patients, detailed inquiry for their first onset time,level, treatment condition, relapse situation, other diseases, other drugs, relapse time, death time, and the like, and registration for survival time and state, a result shows that average survival time and progression free survival of high expression patients are obviously shorter than those of low expression or no expression patients and are related to reactivity of temozolomide; thus, LNC_004208 is a molecular marker related to glioma prognosis; IncRNA LNC_004208 is high in expression; prognosis of patients is poor.

The invention discloses a 2-substituent-7-fluorine-4-aromatic mixed base quinazoline derivant with a novel structure and a preparation method and the use of the derivant in preparation of anti-glioma drug composite. The general combining route includes utilizing 4-fluorine-o-aminobenzoic acid 1 as a general raw material, conducting cyclization to obtain quinazolinone 2, conducting chloro to obtain a key intermediate 3, enabling the intermediate 3 and aniline (phenol or benzene sulfur) compounds to be concentrated, and conducting three steps of reaction (a, b and c) to obtain a compound of a target product 4. Considering that 4-aniline-quinazoline compound has wide biological activity, especially salient antitumor activity, the inventor observes and combines a series of novel 2-substituent-7-fluorine-4-substituent quinazoline derivants in screening of glioma cell lines (U251, U87 and U172). The derivants show good antitumor activity and have wide prospect in treatment of brain tumors.

The invention discloses a bridge molecule 1-siRNA interference sequence and a fusion expression vector thereof, and belongs to the technical field of biology. A fragment of synthesized bridge molecule 1-siRNA interference sequence can reduce the expression of bridge molecule 1 protein, and generate inhibiting effect on cellular infiltration and diffusion function participated by the bridge molecule 1 protein; and after transfecting a human glioma cell line, the bridge molecule 1-siRNA fusion expression vector can specifically degrade bridge molecules 1mRNA complemented with the fusion expression vector, inhibit in vitro migration capability and chemotactic capability of malignant glioma LN-229 cells, inhibit in vitro adhesive capability and invasion capability of the malignant glioma LN-229 cells, reduce infiltration and diffusion capabilities of tumor cells, and provide a feasible technological measure for gene therapy of tumor.

The invention discloses a construction method of a glioma cell line suitable for two-photon living imaging. The construction method comprises the following steps: constructing a glioma cell in-situ transplantation animal model through glioma cells, and researching the dynamic development change of the glioma cells in the brain of a mouse by virtue of a two-photon living body imaging technology. The GL261-ZsGreen glioma cells obtained through transformation can be successfully used for constructing a glioma in-situ transplantation living animal model, the positions of tumor cells can be clearlyobserved in the imaging observation process, cell-level examination can be accurately performed when the GL261-ZsGreen glioma cells are applied to the research field, the glioma boundary can be obviously distinguished, and a potential means is provided for effectively and accurately excising tumors. Each proliferated GL261-ZsGreen cancer cell is provided with a green fluorescence label, so that single cancer cells subjected to dispersive metastasis can be accurately positioned, and a possible scheme is provided for further researching the diffusion of cancer cells and the accurate treatment of glioma.

The invention discloses an aquaporin 4-siRNA interfering sequence, its fusion expression vectors and a medicinal use of the fusion expression vectors, and belongs to the biopharmaceutical field. In the invention, an aquaporin 4-siRNA interfering sequence is designed and fusion expression vectors of the aquaporin 4-siRNA interfering sequence are synthesized. After the fusion expression vectors are transfected into human glioma cell lines, the fusion expression vectors can degrade specifically aquaporin 4mRNA which is complementary with the fusion expression vectors, decrease the expression of an aquaporin protein 4 in a human glioma cell, inhibit effectively a migration capacity, an adhesive capacity and an invasion capacity of human glioma cells and have effects of inhibiting the infiltration and the diffusion of human glioma cells thus provide a feasible technical means for a gene therapy utilized for tumor patients.

The invention provides application of eupatilin or a computer of eupatilin in preparing a drug composition for treating or preventing glioma. Treating or preventing the glioma is achieved by inhibiting the cellular activity of a glioma cell line by the eupatilin, or treating or preventing the glioma is achieved by inhibiting proliferation of the glioma cell line by the eupatilin, or treating or preventing the glioma is achieved by inhibiting the cyclical change of tumor cells by the eupatilin, or treating or preventing the glioma is achieved by inhibiting cell migration of the tumor cells by the eupatilin, or treating or preventing the glioma is achieved by inhibiting invasiveness of the tumor cells by the eupatilin. The application overcomes the severe shortcomings of single drug and drugresistance in the existing treatment or prevention of the 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.

Ferroptosis (cell death mediated by iron-dependent lipid peroxide accumulation) results from lipid peroxidation of phospholipids containing polyunsaturated fatty acyl moieties. Glutathione, the key cellular antioxidant capable of inhibiting lipid peroxidation via the activity of the enzyme glutathione peroxidase 4 (GPX-4), is generated directly from the sulfur-containing aminoacid cysteine, and indirectly from methionine via the transsulfuration pathway. Cysteine and methionine deprivation (CMD) in the diet can synergistically increase RSL3-mediated cell death and lipid peroxidation in both murine and human glioma cell lines and in ex-vivo organotypic slice cultures. A cysteine-depleted, methionine-restricted diet can improve survival in an syngeneic orthotopic murine glioma model. This CMD diet leads to profound in-vivo metabolomic, proteomic and lipidomic alterations, leading to improvements in the efficacy of ferroptotic therapies in glioma treatment with a non-invasive dietary modification.

The present invention relates to molecular biology. Up to now, only twenty odd kinds of cancer inhibiting genes have been obtained and they have no the characteristic of containing the structural domain similar to acyl group carrying protein. The novel gene of the present invention, p40, has cDNA whole length of 2024 bp and complete reading frame, encodes protein containing 357 amino acid residues of molecular weight 40 kD, is one difference expressing gene for the normal brain tissue high expression, glioma tissue and glioma cell low expression or no expression, and is one very good cancer inhibiting gene capable of inhibiting the growth of glioma cell.

The invention relates to a method for researching a function of promoting brain glioma proliferation by an MDK gene and application of the MDK gene. The method comprises the following steps: (1) analyzing MDK expression of a glioma cell line through RT-qPCR, (2) carrying out lentivirus-mediated overexpression and MDK knockout, (3) interfering the influence of MDK gene expression on glioma cell proliferation, and (4) analyzing and detecting the conditions of P-PI3K, PI3K, P-Akt, Akt, p-ERK, N-cadherin, vimentin and beta-catenin in the glioma cell line which interferes with MDK gene expression through Western blot. The PI3K / AKT pathway is a glioma cell proliferation mechanism mediated by the MDK. The invention provides a new thought for treating glioma, and provides a new way for researching glioma drug treatment targets.

The present invention provides a TOP2A inhibition by temozolomide useful for predicting glioblastoma patient's survival. Glioblastoma (GBM) is the most common, malignant primary adult brain tumor. The conventional treatments for GBM, include surgery, radiation, and chemotherapy which have only modestly improved patient survival. The patients with GBM expressing higher TOP2A transcript levels had better prognosis. More interestingly, the present invention reports that temozolomide is an inhibitor of TOP2A activity in vitro. The present invention further shows that siRNA knock down of TOP2A rendered a glioma cell line resistant to temozolomide chemotherapy. Thus it is demonstrated for the first time that temozolomide is a TOP2A inhibitor and establishes that TOP2A transcript levels determines the chemosensitivity of glioblastoma to temozolomide therapy thus explaining the very high levels of TOP2A transcript being a good prognostic indicator in GBM patients receiving temozolomide chemotherapy.

The invention discloses application of combination of a low-temperature plasma and metformin, in particular to application of the combination of the low-temperature plasma and metformin to in-vitro non-therapeutic induction of glioma cell death. The application of the combination of the low-temperature plasma and the metformin to in-vitro non-therapeutic induction of glioma cell death shows that the combination of the low-temperature plasma and the metformin has an obvious synergistic inhibition effect on glioma cell lines U251 and U87 cultured in vitro, and can remarkably induce cell death. The application is used for non-disease treatment, but for in vitro studies, through the scheme of the application of the combination of the metformin and the low-temperature plasma to inducing gliomadeath, a new strategy can be provided for researching the application of the combination of the low-temperature plasma and the metformin to glioma treatment, and a new thought is expected to be provided for designing a new product or a new scheme for treating glioma.

The present invention relates the application of a human source dcf1 gene in the inhibition of U251 glioma cell line proliferation and in the induction of U251 glioma cell line apoptosis. The present invention makes judgments for dcf1-induced U251 cell line apoptosis by the methods of immune electron microscope, atomic force microscope, CCK8 proliferation detection, JC-1 staining, and nude mouce tumor heterotopic transplantation. The results show that: the dcf1 causes mitochondrial structure lesion and membrane potential reduction by locating in mitochondria, thereby causing apoptosis-related gene expression change, and eventually leading to apoptosis. The nude mouce experiments show that the dcf1 can significantly reduce glioma tumor volume and inhibit tumor growth.

The invention discloses application of psoromic acid in the preparation of medicine for treating brain glioma and acute myeloid leukemia. The psoromic acid plays an obvious role in inhibiting the growth of a human brain glioma cell line U87MG and a human erythroid leukemia cell line TF-1. The psoromic acid belongs to natural products and has the characteristics of low toxic or side effects and high bioavailability when the psoromic acid is used for treating brain glioma and acute myeloid leukemia, thereby having certain clinical use value.

The invention discloses a cytoskeletal binding protein siRNA (small interfering ribonucleic acid) interfering sequence, a fusion expression vector thereof and medical application of the same, belonging to the field of biological pharmacy. The invention designs a segment of cytoskeletal binding protein siRNA interfering sequence, and synthesizes the fusion expression vector of the cytoskeletal binding protein siRNA interfering sequence; after the fusion expression vector is transfected into a human glioma cell line, the fusion expression vector can specifically degrade the cytoskeletal binding protein messenger RNA (mRNA) complementary to the fusion expression vector to reduce the expression of the cytoskeletal binding protein in the human glioma cells; and the fusion expression vector can effectively inhibit the migration, adhesion and invasion abilities of the human glioma cells, has an effect on inhibiting the human glioma cellular infiltration and metastasis, and provides a feasible technical means for gene therapy for tumor patients.

The invention discloses combined application of low-temperature plasma and ascorbic acid, and particularly relates to combined application of a culture medium irradiated by the low-temperature plasmaand the ascorbic acid in in-vitro non-therapeutic induction of glioma cell death. It is shown that the culture medium irradiated by the low-temperature plasma and the ascorbic acid are combined to have an obvious synergistic inhibition effect on glioma cell lines U251 and U87 cultured in vitro, and cell death can be remarkably induced. Through the scheme provided by the invention, a new strategy can be provided for researching the combined application of low-temperature plasma and ascorbic acid in glioma treatment, and a new thought is expected to be provided for designing a new product or a new scheme for treating glioma.

The invention discloses a new application of isojacareubin. The new application is meant that isojacareubin as an active ingredient is used in preparation of an antitumor pharmaceutical preparation. Pharmacological tests prove that, isojacareubin has an obvious inhibition effect on growth of U87 human brain glioma cell lines, BXPC-3 human pancreatic cancer cell lines, NCI-2126 human lung cancer cell lines, PANC-1 human pancreatic cancer cell lines, A549 human non small cell lung cancer cell lines, AGs human gastric cancer cell lines, A375 human melanoma cell lines, MCF-7 human breast cancer cell lines, MDA-MB-231 human breast cancer cell lines and SMMC-7721 human liver cancer cell lines, has significant antitumor activity, can be expected to be used as the active ingredient for the preparation of the antitumor pharmaceutical preparation, and has medicinal prospects.