93 results about "Oxidative phosphorylation" patented technology

The invention belongs to the field of biological medicine, and particularly relates to PGK1 K17 site succinylation modification and application. Experiments show that the 17-site lysine of the PGK1 protein has succinylation modification (PGK1 K17su), and the existence of the modification is confirmed through a specific succinylation modified antibody for the first time. Further, it is found that PGK1 K17su can weaken lung cancer cell oxidative phosphorylation and promote glycolysis metabolism by inhibiting lung cancer cell mitochondrial generation, and functional experiments prove that PGK1 K17 succinylation modification promotes proliferation and migration of lung cancer cells.

The invention discloses an application of an engineered exosome rich in SIRT3 in preparation of a medicine for improving mitochondrial dysfunction. The method comprises the following steps: screening to obtain a polypeptide molecular gel G12 targeting HSP60, forming a fusion protein SIRT3-G12 from the G12 and SIRT3, constructing a recombinant plasmid for expressing the fusion protein, transfecting cells, culturing, and extracting an exosome, thereby obtaining the engineering exosome SIRT3-Exo rich in SIRT3. The SIRT3-Exo is used for treating mitochondrial dysfunction, and the research shows that the SIRT3-Exo can remarkably promote mitochondrial oxidative phosphorylation, promote expression of cell antioxidant enzymes and deacetylation of FOXO3a, enhance the antioxidant capacity of cells and remove ROS in the cells, and has the effect of promoting mitochondrial function recovery. The problem that SIRT3 cannot be used for treating mitochondrial dysfunction through exosomes is solved, and good application prospects are achieved.

The invention discloses a self-assembled PROTAC nano material based on natural product mitochondria targeting, which is a nano particle prepared from mitochondria targeting molecules, a photosensitizer and PROTAC as raw materials through a nano precipitation method. The mitochondrial targeting molecule is berberine, the photosensitizer is hypericin, and the PROTAC is dBET57; the ratio of the amount of substance of the dBET57 to the amount of substance of the berberine is (1-10): (1-10), and the ratio of the amount of substance of the dBET57 to the amount of substance of the hypericin is (1-10): (1-10). The nano material can be used for blocking multiple energy metabolism pathways of tumor cells, including glycolysis and oxidative phosphorylation, meanwhile, mitochondria is damaged, ferroptosis is induced, and the anti-tumor capacity of pharmacodynamic molecules is improved; bRD4 in tumor cells and downstream carcinogenic protein c-Myc of the BRD4 can be efficiently degraded. The invention also discloses an application of the nano material in preparation of antitumor drugs.

The invention provides a preparation method and application of CAR-T cells for overexpressing C1QBP, and relates to the field of cell engineering. According to the CAR-T cell overexpressing the C1QBP, the energy metabolism of the cell is optimized by improving the oxidative phosphorylation of mitochondria, the formation of memory-like T cells is promoted, and the anti-tumor activity and long-term durability of the CAR-T cell are enhanced. The cells can survive in a tumor microenvironment for a long time, and the anti-tumor effect of the cells is more durable than that of traditional CAR-T cells. Therefore, a new direction is provided for research and development of cellular immunotherapy.

The invention discloses an application of an engineered exosome rich in RHOT1 in preparation of a medicine for improving insulin resistance. The engineering exosome RHOT1-Exo rich in RHOT1 is obtained by the following steps: screening to obtain a polypeptide P15 targeting CD81, forming a recombinant protein RHOT1-P15 from the P15 and RHOT1, then constructing a recombinant plasmid for expressing the recombinant protein, transfecting cells, culturing, and extracting the exosome, thereby obtaining the engineering exosome RHOT1-Exo rich in RHOT1. The RHOT1-Exo is used for treating insulin-resistant cells, and the research shows that the RHOT1-Exo can effectively improve the ATP content of mitochondria, improve the oxidative phosphorylation level, enhance the antioxidant enzyme activity of cells and reduce ROS (reactive oxygen species), finally improve the mitochondrial network structure and improve the expression of insulin signal channel related proteins, and can be used for treating insulin-resistant cells. The obvious mitochondrial function repairing potential and the insulin resistance improving effect are shown. According to the invention, the RHOT1 protein is successfully applied to the treatment of insulin resistance in the form of exosome, and a scientific strategy is provided for the application of the medicine for clinically treating insulin resistance.

A method of generating a hematopoietic cell, including providing a source cell and treating the source cell with a metabolic regulator that directs the source cell to preferentially use glycolysis or oxidative phosphorylation and / or cholesterol biosynthesis, wherein the source cell is differentiated into a GPA+ erythroid cell or a CD45+ non-erythroid cell. In some examples, the source cell is selected from the group consisting of a hemogenic endothelial (HE) cell, a iPS cell such as a differentiating iPS cell, a cell directly reprogrammed to a known pre-cursor of a hematopoietic cell, a cell directly reprogrammed to a hematopoietic cell or precursor of a hematopoietic cell, a reprogrammed cell that is subsequently further reprogrammed to a hematopoietic cell or precursor of a hematopoietic cell, an adult hematopoietic cell derived from bone marrow or mobilized peripheral blood and a neonatal hematopoietic cell derived from cord blood or prenatal tissue (e.g. placenta). Some examples involve metabolically regulating a lipid biosynthesis pathway with an inhibitor of the lipid biosynthesis pathway or metabolically regulating a histone acetylation pathway with an inhibitor of the histone acetylation pathway.

The invention discloses a probe combination for detecting a mitochondrial respiratory chain super complex based on a proximity ligation assay and a hybridization chain reaction and application, and belongs to the field of probe detection. Two adjacent protein subunits capable of reflecting the structural integrity of the hypercomplex are determined as bases, the antigen-antibody combination principle is utilized to promote the antigen-antibody which recognizes and combines the bases to initiate proximity ligation reaction (PLA) due to nucleic acid labeling, cascade amplification of detection signals is realized according to the hybridization chain reaction (HCR) principle, and the detection sensitivity of the hypercomplex is improved. The activity of the oxidative phosphorylation system is judged through the structural integrity of the super-complex, the defects and limitation of a traditional detection method are overcome, and rapid, high-sensitivity and accurate detection on the structure of the super-complex is achieved. Meanwhile, the cells are fixed on a 96-hole fluorescent plate, and the structural integrity of the mitochondrial hypercomplex is detected by using a multifunctional microplate reader, so that parallel detection on 96 samples at the same time is finally realized, and digitization and high throughput of detection are realized.

The invention belongs to the technical field of biological medicine, and relates to pharmaceutical application of an oxidative phosphorylation inhibitor, in particular to application of the oxidative phosphorylation inhibitor in preparation of an immunomodulatory drug, and the immunomodulatory drug has the advantages that the function damage of newborn myeloid-derived suppressor cells caused by antagonism BCG (bacillus calmette guerin) vaccination is inhibited, and the immunomodulatory effect is improved. The compound is used for preventing or treating neonatal immune-related diseases caused by bacillus calmette guerin vaccine inoculation. The invention finds that the BCG can cause damage to the immunosuppression function of the MDSC of the suckling mouse through up-regulation oxidative phosphorylation, and the negative effect caused by inoculation of the BCG can be reversed by using the OXPHOS inhibitor, so that the immunosuppression function of the MDSC of the suckling mouse is successfully recovered in an in-vivo and in-vitro model, and the immune-related adverse reaction caused by inoculation of the BCG is expected to be improved.

The invention discloses an application of a pyruvate dehydrogenase kinase (PDKS) inhibitor in preparation of a composition for treating Alzheimer's disease (AD), and particularly discloses an application of the PDKs inhibitor in preparation of the composition for treating the AD. According to the invention, the level of oxidative phosphorylation (OXPHOS) of microglial cells is obviously enhanced, the inflammatory response of the microglial cells is effectively reduced, the migration and aggregation capabilities of the microglial cells are obviously improved, the capability of the microglial cells to phagocytize and degrade extracellular beta-amyloid protein (A beta) plaque is obviously enhanced, the cognitive function defect of AD model mice is effectively improved, and the application of the microglial cells in the treatment of the AD model mice is promoted. The preparation is simple, and the application is wide.

A device for activating the mitochondrion, wherein negative charge and reactive oxygen are delivered from outside to the mitochondrion via a negative charge and reactive oxygen delivery unit to serve as material for the mitochondrial redox reaction; and, wherein a calcium ion channel stimulation unit can stimulate an in vivo calcium ion to transport a protein across a calcium ion on an inner membrane of the mitochondrion into a matrix space of the mitochondrion, whereby an influx of the calcium ion promotes the depolarization of the mitochondrion and increases the activity of mitochondrial oxidative phosphorylation.

The disclosure provides a hybrid membrane camouflaged nanomedicine loaded with oxidative phosphorylation inhibitor and preparation method thereof. The nanomedicine comprises an inner core and an outer shell coated on the periphery of the inner core. The inner core is a ROS-responsive drug-loaded nanoparticle, and the drug loaded by the ROS-responsive nanocarrier is an oxidative phosphorylation inhibitor. The outer shell is a hybrid membrane of mitochondrial membrane and cancer cell membrane. The nanomedicines can cross the BBB and reach tumor sites by the homologous targeting of cancer cell membrane, and then they can homologously target and enter mitochondria by the mitochondrial membrane. Subsequently, under the high-level ROS environment of the mitochondria, the ROS responsive drug-loaded nanoparticle releases the oxidative phosphorylation inhibitor due to the swell and degradation of the inner core, so that the safe and efficient targeted GBM therapy is achieved.

The invention discloses a polyphosphate-metal nano-composite as well as a preparation method and application thereof, and belongs to the technical field of biological medicines and nano-materials. The polyphosphate-metal nano-composite is formed by self-assembly of polyphosphate and metal ions under the coordination action; wherein the chain length of the polyphosphate is 20 to 75. According to the invention, divalent metal ions are introduced, so that polyphosphate and metal ions form a spherical nano-composite through coordination self-assembly, the composite can be absorbed by tumor cells and degraded under an acidic condition, released polyphosphoric acid is separated through unique Ca < 2 + > phase, Ca < 2 + > is enriched around mitochondria, and the function of tumor treatment is realized. And tumor cell metabolism reprogramming is caused to be dominated by oxidative phosphorylation, so that copper death and immunoregulation are induced, and a triple synergistic anti-tumor effect is realized.

The invention belongs to the technical field of biological medicines, and particularly relates to an application of LAP3 and an agonist thereof in macrophage immune inflammation mediated diseases. The invention provides application of leucine aminopeptidase 3 or leucine aminopeptidase 3 agonist substances in preparation of drugs for prevention, treatment and / or adjuvant treatment of macrophage immune inflammation mediated diseases. According to the invention, it is found for the first time that the expression level of LAP3 in macrophages is increased under an acute stress condition, and the limiting effect of LAP3 on generation and development of sepsis and acute hepatitis is disclosed; the invention discloses that the knockout of the LAP3 can remodel a macrophage metabolic network, reduce oxidative phosphorylation, promote ROS (reactive oxygen species) production and activate TAK1, thereby promoting the activation of a downstream inflammation signal channel and finally promoting macrophage inflammation. A new target spot and a theoretical basis can be provided for clinical diagnosis and treatment of macrophage-mediated inflammation by illuminating the effect of LAP3 on regulating and controlling macrophage inflammation and a molecular mechanism of LAP3.

The invention discloses a novel application of total glucosides of paeony in preparation of a medicine for treating triple negative breast cancer. In-vitro and in-vivo experiments prove that the total glucosides of paeony can remarkably inhibit proliferation, migration and invasion of triple negative breast cancer cells (MDA-MB-231 and MDA-MB-468), reverse an epithelial-mesenchymal transition process and induce cell apoptosis by inducing mitochondrial injury, inhibiting oxidative phosphorylation and activating a mitochondrial apoptosis pathway. In an MDA-MB-231 cell xenotransplantation tumor nude mouse model, the total glucosides of paeony can effectively inhibit tumor growth. Therefore, the total glucosides of paeony can be used for preparing the medicine for treating the triple negative breast cancer, and a new treatment choice is provided for clinic.

The present application relates to the technical field of biomimetic materials, in particular to a multiphase biomimetic mineralized collagen scaffold, a preparation method and application thereof.The preparation method is as follows: type I collagen solution is self-assembled with solid copper sulfide nanoparticles, and through the technology of liquid phase mineralization, intracellular mineralization of collagen fibrils occurs, forming a multiphase biomimetic mineralized collagen scaffold similar to the nanostructure and Young's modulus of natural bone.The scaffold can improve the energy metabolism of cells by regulating the oxidative phosphorylation of bone marrow mesenchymal stem cells, thereby promoting the osteogenic differentiation of the cells; in addition, the scaffold releases copper ions to simulate enzyme activity, catalyzing the generation of a large amount of active oxygen in bacteria, leading to the rupture of the bacterial membrane and the overflow of the contents, thereby achieving the effect of antibacterial.The scaffold can treat simple bone defects or infected bone defects by regulating the energy metabolism of cells and simulating enzyme activity, thereby providing more new methods for the preparation of drugs for realizing bone regeneration and anti-infection in clinic.

The invention discloses an NKT cell, a culture medium and a culture method thereof, and relates to the technical field of cell culture, the NKT cell comprises a basal culture medium, a cell factor combination, a plant extract compound, a metabolism regulator and an antioxidant; wherein the plant extract compound is prepared from astragalus polysaccharide, ganoderic acid, tea polyphenol, asiaticoside and notoginsenoside R1, and the mass ratio of the astragalus polysaccharide to the ganoderic acid to the tea polyphenol to the asiaticoside to the notoginsenoside R1 is (3 to 5) to (1 to 2) to 1 to (0.5 to 1) to (0.5 to 1). According to the NKT cell, the culture medium and the culture method of the NKT cell, through the synergistic effect of the six-membered plant extract compound, the expression of cyclin is promoted, the G1 / S phase conversion is accelerated, and the cell amplification amount is remarkably increased; the ratio of plant extracts and high astragalus polysaccharide are dynamically adjusted, so that cell proliferation and induced differentiation of high ganoderic acid are promoted, cells are forced to turn to efficient-productivity oxidative phosphorylation metabolism in cooperation with 2-deoxyglucose, and the cell multiplication time is shortened.

The invention belongs to the technical field of biological medicines, and particularly relates to a novel application for regulating and controlling de-lactation acylation of a K309 site of an autophagy-associated protein 7 (ATG7) based on a silent information regulatory factor 1 (Sirt1) activator and treating tumors through targeted metabolism reprogramming. The key effect of lactoacylation modification of the K309 site of ATG7 in tumor cell metabolism reprogramming is disclosed for the first time, and it is proved that a Sirt1 activator inhibits the Warburg effect through lactoacylation, enhances mitochondrial oxidative phosphorylation (OXPHOS) and triggers metabolic stress and tumor cell death. Cell experiments prove that the Sirt1 activator has a remarkable killing effect on tumor cells with high ATG7-K309 lactoacylation level, and a new strategy is provided for precise treatment.

The present invention provides fungicidal combination comprising: (i) an amount of a compound of Formula Iand (ii) an amount of at least one fungicide (A) selected from the group consisting of pyrimidines, antibiotics, anilinopyrimidines (AP), aromatic hydrocarbons, aryl-phenylketones, azanaphthalenes, benzamides, benzenesulfonamides, benzo-thiadiazoles (BTH), carboxylic acid amides (CAA), carbamates, cyanoacetamideoxime, dicarboximides, dithiolanes, growth regulators, guanidines, heteroaromatics, inorganics, methyl benzimidazole carbamates (MBC), melanin biosynthesis inhibitors (MBI), membrane disruptors, organo tin compounds, oxysterol binding protein homologue inhibition (OSBPI), phenylamides (PA), phenylacetamides, phenylureas, phosphonates, polyoxins, phenylpyrroles, uncouplers of oxidative phosphorylation, dithianon, sulphur, bordeaux-mixture, thiram, zineb, ziram, famoxadone, fenamidone, pyribencarb, ametoctradin, diniconazole, penconazole, triadimefon, triadimenol, triflumizole, bromuconazole, imazalil, tridemorph, flutolanil, thifluzamide and metominostrobin.

The invention discloses a nano blocker for hyaluronic acid energy metabolism of a targeted CD44 receptor as well as a preparation method and application of the nano blocker. The nano blocker is a nano preparation obtained by modifying a polylactic acid-glycolic acid copolymer (PLGA) with hyaluronic acid (HA) and then coating the PLGA with nebivolol hydrochloride and 3-bromopyruvic acid, and the nano preparation is marked as NBP-coated PLGA-HA. According to the CD44 receptor targeted hyaluronic acid energy metabolism nano blocking agent disclosed by the invention, bidirectional blocking of basic respiration of tumor cells is realized by using a loaded mitochondrial oxidative phosphorylation (OXPHOS) inhibitor nebivolol hydrochloride and a glycolysis inhibitor 3-bromopyruvic acid; meanwhile, effector immune cells are synergistically enhanced to maintain systemic anti-tumor immunity, high efficiency and safety are shown in in-vitro and in-vivo experiments, and concept paradigm transformation is provided for nano-drug mediated tumor treatment based on energy metabolism.

The invention provides an application and a method of GSH in promoting mature differentiation of hiPSC-CMs, and the method is characterized in that in the process of directionally differentiating the hiPSC-CMs into the hiPSC-CMs, an effective dose of GSH is added into a differential medium, and the optimal concentration is 20-100 [mu] M. According to the invention, through simple and economical exogenous supplement of GSH, maturation of hiPSC-CMs is systematically promoted from multiple dimensions, including enhancement of intracellular anti-oxidation defense capability; energy metabolism is promoted to be converted from glycolysis to oxidative phosphorylation; up-regulating expression of cardiac muscle cell specific structural protein and calcium ion channel related genes; mitochondrial biological generation and functions are promoted; and the cell morphological structure is induced to develop to a mature phenotype. The method is simple and convenient to operate and high in biocompatibility, the hiPSC-CMs with mature functions can be stably obtained, and a high-quality cell source is provided for application of the hiPSC-CMs in the fields of heart disease modeling, drug cardiotoxicity screening and the like.

The invention discloses application of a membrane-bound O-acyltransferase structural domain 7 (Mboat7) in preparation of a medicine for treating myocardial infarction, and belongs to the technical field of biology. A research result shows that in a mouse myocardial infarction model, compared with a control group mouse, the death rate of a myocardial cell specific Mboat7 gene overexpressed mouse is reduced, the infarction area is remarkably reduced, and the cardiac function is remarkably improved; the overexpressed Mboat7 gene can relieve mitochondrial damage of myocardial cells under the hypoxia condition and improve the mitochondrial oxidative phosphorylation function. Particularly, overexpression of the Mboat7 gene can improve damage of mitochondria in myocardial tissues of mice suffering from myocardial infarction. The results show that Mboat7 gene overexpression can relieve myocardial damage after myocardial infarction so as to delay the progress of heart failure, and Mboat7 or an expression promoter thereof can be used for preparing the medicine for preventing, relieving and / or treating myocardial infarction.

The invention belongs to the technical field of medicines, and particularly relates to application of arginine in repairing skeletal muscle injury caused by monensin poisoning. It is found for the first time that arginine can remarkably recover the normal function of skeletal muscle mitochondria and the normal polymerization capacity of microtubules by up-regulating the expression level of mitochondrial oxidative phosphorylation (OXPHOS) protein complex and regulating microtubule polymerization kinetics and reversing monensin-induced skeletal muscle mitochondrial dysfunction and microtubule network disintegration; the method provides a theoretical basis for clinical transformation, and has good practical application value.

The present application relates to the technical field of biological medicine, and particularly relates to application of a nucleic acid vector encoding a macrophage monocarboxylate transporter MCT1 in preparation of a pharmaceutical composition for promoting corneal nerve regeneration and recovery of corneal sensitivity after corneal nerve injury. The present application finds that after corneal nerve injury, increasing the level of macrophage MCT1 can drive the change of the metabolic mode of macrophages to the direction of enhanced oxidative phosphorylation and reduced glycolysis, reduce the expression of local pro-inflammatory related factors, and increase the level of pro-regeneration factors and neurotrophic factors, thereby improving the regeneration of corneal nerve structure and the recovery of sensory function. Therefore, a macrophage-targeted or macrophage-biased expression vector containing a nucleic acid sequence encoding MCT1 can be used for preparation of a pharmaceutical composition for treating corneal nerve injury.

The present invention discloses a tumor energy depletion nanoassembly and its preparation method and application, which belongs to the technical field of new excipients and new dosage forms for combined treatment of pharmaceutical preparations. The tumor energy depletion nanoassembly is co-assembled by a mitochondrial oxidative phosphorylation inhibitor and a glycolysis inhibitor through intermolecular forces, and modified with a PEG modifier; the molar ratio of the mitochondrial oxidative phosphorylation inhibitor and the glycolysis inhibitor is 10:1 to 1:10, and the mass ratio of the sum of the mitochondrial oxidative phosphorylation inhibitor and the glycolysis inhibitor to the PEG modifier is 10:90 to 90:10. The tumor energy depletion nanoassembly of the present invention has a high drug loading capacity, good stability, and low toxic and side effects, providing a new strategy for the assembly of homologous synergistic drug nanoparticles, and providing an effective nano-platform for the development of carrier-free hybrid nanoassemblies and energy depletion-driven combined tumor treatment.

The invention relates to the technical field of tumor cell metabolism analysis, and discloses a tumor cell metabolism comprehensive evaluation system based on mitochondrial function indexes. Comprising a multi-dimensional detection module used for acquiring detection data of mitochondrial membrane potential, active oxygen and cell ATP energy cycle products of tumor cells; the control module is in communication connection with the multi-dimensional detection module and is configured to receive the detection data and establish a comprehensive analysis model containing energy metabolism, oxidative stress and mitochondrial autophagy related parameters based on the bidirectional regulation and control relationship between the HIF-1alpha and mitochondria so as to perform correlation analysis and weight calculation on the detection data, and the weight of the comprehensive analysis model is calculated; generating a comprehensive evaluation index reflecting the metabolic state of the tumor cells; and outputting a metabolic characteristic analysis report corresponding to the comprehensive evaluation index, wherein the metabolic characteristic analysis report comprises comprehensive evaluation results of the tumor cell mitochondrial oxidation phosphorylation level, mitochondrial autophagy activity and oxidative pressure.

The present invention relates to a disubstituted adamantyl derivative or a pharmaceutically acceptable salt thereof, a pharmaceutical composition for anti-cancer containing the same as an active ingredient, and a kit. The disubstituted adamantyl derivative of the present invention inhibits the growth of cancer cells by targeting mitochondrial ETC complex I and disrupting cancer cell metabolism, and thus can be effectively used as a pharmaceutical composition for anti-cancer. This composition is a potent cancer therapeutic agent that depends on oxidative phosphorylation for ATP generation.

The invention provides an application of transporter ABCA8 positive cancer related fibroblast as a marker in preparation of a kit for diagnosing SETD2 defect pancreatic cancer. The invention also provides an application of the transporter ABCA8 positive cancer-related fibroblast as a marker for diagnosing pancreatic cancer with a high oxidative phosphorylation metabolism characteristic. The invention also provides application of the transporter ABCA8 as a target spot in preparing and screening medicines for treating the SETD2 defect pancreatic cancer. According to the invention, it is identified for the first time that a new CAF subgroup with an ABCA8 marker and rich in lipid exists in SETD2-deficient pancreatic cancer, and the subgroup CAF provides lipid for tumor cells through ABCA8 transporter protein, so that OXPHOS of tumor cell mitochondria is enhanced, and tumor progression is maintained.

The present invention relates to a method for activating the mitochondrion, wherein mainly negative charges and reactive oxygen species are supplied to the mitochondrion from the outside via a negative charge and reactive oxygen species delivery unit to serve as material for the mitochondrial redox reaction. A calcium ion channel stimulation unit stimulates an in vivo calcium ion to transport the protein across the calcium on the inner mitochondrial membrane into a mitochondrial matrix space, such that the influx of calcium ions promotes mitochondrial depolarization and increases the activity of mitochondrial oxidative phosphorylation. This enhances mitochondrial activation and ATP production.

The invention discloses clinical application of a metabolic immune and Dai medicine composition in treatment of cancer, the composition comprises: a composition for regulating and controlling tumor cell metabolism, including 2-deoxy-D-glucose, a glycolysis inhibitor, an oxidative phosphorylation inhibitor, a pyruvate dehydrogenase kinase inhibitor, a polyphenol compound and green tea polyphenol; at least one immunomodulator; at least one chemotherapeutic agent; the clinical application of the metabolic immune combined Dai medicine for treating the cancer is realized through action mechanisms in multiple aspects, including influence on the metabolic activity of tumor cells, enhancement of the effect of an immune system, enhancement of the effect of a chemotherapy medicine and leveling of four towers and five components, so that toxin is eliminated, qi and blood are straightened out, resistance is enhanced, and the clinical application of the metabolic immune combined Dai medicine for treating the cancer is realized. The functions of four towers and five components are balanced and coordinated, so that the aim of treating cancers is fulfilled.