18 results about "Resistant cell" patented technology

The application discloses application of Ophisaurus apodus in preparation of a drug for reversing drug resistance of gastric cancer and belongs to the technical field of medicines. The application can reduce tumor volume and size, promote drug resistance cell apoptosis, and reverse the chemotherapeutic drug resistance of a nude mouse with gastric cancer by jointly using Ophisaurus apodus in different parts of the body and cisplatin, by down-regulating P-gp, MRP1 and Bcl-2 protein expression, and by up-regulating Bax protein expression. The effect of the tail + cisplatin group is the most significant.

The application discloses a butyl tin-cycloiridium phenanthroline complex with an aggregation-induced emission (AIE) property, a preparation method of the complex and anticancer application of the complex. The structural formula of the complex is shown as formula (I), and R is one of hydrogen, a phenyl group, a p-tolyl group, a p-bromophenyl group, a p-fluorophenyl group, a biphenyl group, a triphenylamine group, a carbazole group, a tetraphenyl ethene group and a triphenylbenzene group. The growth inhibition rates of the target compound on human alveolar basal epithelial carcinoma cells (A549) and cisplatin-resistant cells (A549 / DDP), cervical cancer cells (Hela) and human lung normal epithelial cells (BEAS-2B) are tested, and it is found through comparison that the target compound shows potential anticancer activity. In addition, the target compound shows unique AIE emission characteristics. The target compound mainly targets the lysosomes of A549 cells, and influences the mitochondria to cause the decline of the mitochondrial membrane potential, thereby showing anticancer activity.

The application discloses application of a Blautia in preparation of a drug for enhancing sensitivity of colorectal cancer to oxaliplatin, B-CM can significantly enhance OXa cytotoxicity on drug-resistant colorectal cancer cells, inhibit proliferation, clone formation, migration and invasion ability. Combination therapy can synergistically induce apoptosis, although the expression of MDR1 in drug-resistant cells is up-regulated, but the combination of B-CM and OXa can significantly reduce the mRNA and protein levels. In vivo experiments show that B-CM enhances the tumor inhibition effect of OXa, which is related to the reduction of the expression of Ki-67 and MDR1 in tumor tissues. Further, it can be shown that the soluble factor derived from Blautia can reverse the drug resistance of colorectal cancer to oxaliplatin by down-regulating MDR1 and inhibiting epithelial-mesenchymal transition. This shows that Blautia-derived metabolites are a promising new adjuvant strategy to overcome chemotherapy resistance of colorectal cancer.

Bispecific antibody against EGFR and c-Met. The heterodimeric interaction between the EGFR binding arm and the c-Met binding arm of the bispecific antibody is stronger than the interaction of each in the source homodimer by modifying the Fc segment amino acid sequence of the binding arm, so that it can be assembled into a heterodimer in vitro; its effect on inhibiting the proliferation of EGFR and c-Met double-positive tumor cells is stronger than the combination of EGFR monoclonal antibody and c-Met monoclonal antibody, mediates antibody-dependent cellular cytotoxicity (ADCC), promotes target protein internalization and inhibits the proliferation of osimertinib acquired resistant cell lines. Since the prepared bispecific antibody is simple to prepare, stable in structure, and can obtain a pure bispecific antibody by in vitro assembly, it is expected to better meet the clinical treatment needs, and therefore has a good market prospect.

The present application relates to the field of biological medicine, and particularly relates to a drug composition for reversing lenvatinib drug resistance and application thereof. One object of the present application is to provide a drug composition containing cubenix and lenvatinib. Through the synergistic effect of cubenix and lenvatinib, the inhibitory effect on liver cancer lenvatinib drug-resistant cells is significantly improved, at the same time, the lenvatinib drug-resistant cell colony formation can be significantly inhibited, the lenvatinib drug-resistant cell apoptosis is promoted, and a better tumor inhibition effect is achieved in the liver cancer tumor-bearing mouse experiment.

This invention relates to the field of biomedicine, specifically to a synergistic and targeted epigenetic pharmaceutical composition for the treatment of lung cancer. In studies of drug-resistant lung cancer cells, it was found that overexpression of the NSUN7 gene in drug-resistant lung cancer cells can inhibit MZF1. L The expression of MZF1 also promotes S When the expression of NSUN7 gene was suppressed, no promotion of MZF1 was found. L The expression of MZF1 can be suppressed at the same time. S The expression of NSUN7 gene was inhibited, meaning no opposite result was obtained. However, when NSUN7 gene expression was inhibited and EGFR-TKI inhibitors were administered to drug-resistant lung cancer cells, MZF1 cells in drug-resistant lung cancer cells showed a positive result. L Upregulation, MZF1 S Decreased expression of NSUN7 leads to the transformation of drug-resistant lung cancer cells into drug-sensitive cells. Therefore, interfering with NSUN7 in combination with epigenetic drugs to regulate the alternative splicing of methylation-sensitive transcription factors can increase the specificity of regulatory targets and synergistically enhance the in vitro and in vivo antitumor effects.

This invention belongs to the field of biomedical technology and discloses a paclitaxel reduction-responsive prodrug micelle with high encapsulation efficiency and its preparation method. The paclitaxel-loaded reduction-responsive prodrug micelles prepared in this invention use biocompatible polyethylene glycol (mPEG) and the drug indomethacin (IND) as the hydrophilic and hydrophobic ends of the micelles, respectively, exhibiting synergistic antitumor effects. Simultaneously, it can reverse multidrug resistance to paclitaxel, increase the sensitivity of drug-resistant cells to paclitaxel, and introduce disulfide bonds between the hydrophilic and hydrophobic ends as a linker arm for reduction-sensitive response, responding to the high concentration of GSH in tumor cells to achieve targeted and precise drug release within tumor cells. This prodrug micelle achieves the goals of solubilizing poorly soluble drugs, tumor targeting, and precise drug release at tumor sites, thus enhancing drug efficacy.

This invention belongs to the field of fungal polysaccharide application technology, specifically relating to a method for preparing and applying polysaccharide from *Boletus globosum*. Crude polysaccharide was extracted from the fruiting body of *Boletus globosum* using hot water extraction, and purified using DEAE-52 cellulose column chromatography. Subsequently, by establishing an alcohol-induced liver injury model, it was found that NOP-1 significantly reduced ALT and AST levels, while simultaneously decreasing MDA content and increasing SOD activity and GSH levels, indicating that NOP-1 can inhibit lipid peroxidation, enhance the antioxidant defense capacity of hepatocytes, and maintain hepatocyte membrane integrity. A HepG2 cell IR model was constructed using a high-glucose, high-insulin combined induction method, determining the optimal dosage of NOP-1. ‑6 Treatment of HepG2 cells with mol / L insulin for 24 h successfully induced insulin resistance. Glucose consumption experiments in IR HepG2 cells demonstrated that NOP-1 significantly enhanced the glucose consumption capacity of insulin-resistant cells, exhibiting significant in vitro hypoglycemic activity.

The application discloses a lung cancer immunotherapy acquired drug resistance cell strain and application thereof in preparation of a lung cancer PD-1 inhibitor and / or PD-L1 inhibitor acquired drug resistance mouse model. The lung cancer immunotherapy acquired drug resistance cell strain is resistant to the PD-1 inhibitor and the PD-L1 inhibitor, can be used for constructing the lung cancer PD-1 inhibitor and / or PD-L1 inhibitor acquired drug resistance mouse model, and can be used for researching a PD-L1 and PD-1 immunotherapy drug resistance mechanism and simulating changes in a microenvironment in tumor tissue. The application further discloses the lung cancer PD-1 inhibitor and / or PD-L1 inhibitor acquired drug resistance mouse model and a construction method thereof.

This invention discloses the application of CALD1 protein in the preparation of drugs for treating bladder cancer, belonging to the field of biomedical technology. The application of CALD1 protein in the preparation of drugs for treating bladder cancer: This invention, through the construction of drug-resistant cell lines using in vivo animal models and combined with clinical sample analysis, first discovered that CALD1 is highly expressed in cisplatin-resistant bladder cancer cells and is associated with poor patient prognosis, demonstrating that CALD1 is a potential novel target for treating cisplatin resistance in bladder cancer, which is beneficial for further research on the mechanism of tumor chemotherapy resistance caused by abnormal activation of CALD1.

The disclosure relates generally to methods and compositions for performing bone marrow transplants using a non-myeloablative chemotherapeutic agent and chemotherapeutic-resistant cells. Using the methods and compositions described herein, a patient's bone marrow may be reconstituted and the patient avoids adverse side effects, including myeloablation and / or an impaired immune system.

There is provided a drug delivery composition containing an acid-resistant cell that encloses a drug in the cell. In addition, there is provided an acid-resistant cell in which a drug is enclosed in the cell, where the drug is localized in the sac-shaped membrane structure included in the acid-resistant.

The present application belongs to the technical field of biological medicine, and particularly relates to a marker for anti-osteosarcoma chemotherapy resistance and application thereof. The marker for anti-osteosarcoma chemotherapy resistance provided by the present application is SOCS1. The present application also provides application of the marker in preparation of a drug for diagnosing and / or treating anti-osteosarcoma chemotherapy resistance. The present application determines the mechanism of anti-osteosarcoma chemotherapy resistance by studying the action principle and expression mechanism of anti-osteosarcoma chemotherapy resistance, and finds that SOCS1 expression is down-regulated in anti-osteosarcoma chemotherapy resistance cell lines. Therefore, the present application takes SOCS1 as a marker for anti-osteosarcoma chemotherapy resistance, provides a new treatment strategy for osteosarcoma chemotherapy resistance, and has important academic value and good clinical application prospect.

This invention relates to the field of tumor cell model construction and application technology, specifically to a small cell lung cancer DMS114 radiation-resistant cell line model and its construction method and application. This model is derived from small cell lung cancer DMS114 and can better simulate the radiation resistance phenomenon generated during clinical small cell lung cancer radiotherapy. It innovatively adopts a five-step gradient irradiation scheme, which significantly shortens the construction cycle and reduces human and material costs, providing an effective experimental tool for studying the radiation resistance mechanism of small cell lung cancer and screening radiosensitizers.

This application discloses the application of RECQL as a target in the preparation of products for the treatment and diagnosis of gastric cancer, belonging to the field of biomedical technology. Its key technical point lies in providing the application of RECQL as a target in the preparation of products for diagnosing the sensitivity of gastric cancer patients to oxaliplatin chemotherapy or for diagnosing the efficacy and prognosis of patients receiving oxaliplatin. This application, by detecting RECQL gene / protein expression, histone H1.2 binding status, and K637 site lactation level, can efficiently predict patient drug sensitivity, avoiding the toxic side effects and treatment delays of indiscriminate chemotherapy. Targeted methods such as downregulating RECQL activity, blocking related binding, or inhibiting lactation can effectively restore oxaliplatin-induced DNA damage, significantly reverse drug resistance, and improve chemotherapy efficacy. Simultaneously, the key target is clearly identified, facilitating new drug development, and the relevant effects have been verified through in vitro and in vivo experiments, inhibiting the proliferation of drug-resistant cells and reducing tumor volume, laying a solid foundation for clinical translation, and possessing both practical value and translational potential.

The application discloses a use of sildenafil in preparation of an anti-breast cancer drug in combination with tamoxifen, and sildenafil can promote the entry of GAPDH into a nucleus and inhibit the proliferation of tamoxifen-resistant cells (MCF-7TR). The application also discloses an anti-breast cancer drug composition which can inhibit the proliferation of breast cancer tamoxifen-resistant cells (MCF-7TR) and thus reverse the sensitivity of the drug-resistant cells to tamoxifen, and the composition comprises sildenafil and tamoxifen. The application utilizes the targeted reversing effect of sildenafil on breast cancer cells resistant to tamoxifen, so that the breast cancer tamoxifen-resistant cells can be restored to be sensitive to tamoxifen, and a more economical, convenient and effective treatment option is brought to tumor patients.