57 results about "Nuclear translocation" patented technology

The invention belongs to the technical field of cytotoxicity intervention, and particularly relates to application of an inhibitor JSH-23 in preparation of a medicine for preventing and / or treating ovarian toxicity caused by environmental toxin combined exposure. Aiming at the condition that MC-LR and NaNON combined exposure can activate NF-kappa B to induce KK-1 cell nitrification stress and cause mouse ovarian dysfunction, JSH-23 is selected as an intervention agent, and it is found that after KK-1 cells are pretreated by JSH-23, NF-kappa B nuclear translocation induced by the KK-1 cells due to MC-LR and NaNON combined exposure is remarkably inhibited, iNOS protein rising induced by toxin combined exposure is remarkably reduced, and NF-kappa B nuclear translocation induced by the KK-1 cells due to NF-kappa B combined exposure is remarkably inhibited. The increase of the levels of ONOO and 3-NT of nitration stress markers is effectively relieved, which indicates that JSH-23 can participate in the nitration stress of KK-1 cells caused by combined exposure of MC-LR and NaNO2 by inhibiting NF-kappa B activation, and a foundation is laid for screening antidotes after exposure of environmental toxins.

This invention discloses the application and method of a STAT1-targeting inhibitor in the treatment of immune thrombocytopenic purpura (ITP). It employs ivermectin, a STAT1 nuclear translocation inhibitor, and fludarabine, a STAT1 activation inhibitor. By injecting either the activation inhibitor or the nuclear translocation inhibitor, the platelet count in a mouse model of ITP is increased. Fludarabine, a fluorinated nucleotide analog of vidarabine, is non-radioactive and a small-molecule phosphorylation inhibitor. Ivermectin is a small-molecule inhibitor of nuclear translocation mediated by α / β1 introgression protein. Both have high bioavailability and are widely used to treat various hematological diseases with good safety profiles. Their application in treating ITP is safe, effective, and shows high compliance.

The invention relates to application of NMRK2 in regulating and improving myocardial ischemia reperfusion injury, and belongs to the technical field of biological medicine. Based on the lack of medicines for effectively preventing and treating myocardial ischemia-reperfusion injury at present, the invention develops a protection method based on NMRK2 signal regulation and control, specifically, a preparation for enhancing NMRK2 expression or activity is adopted to prepare the medicines for preventing or treating myocardial ischemia-reperfusion injury, and the medicines can systematically enhance the anti-oxidation defense capability of myocardial cells, so that the anti-oxidation defense capability of myocardial cells is enhanced. The tissue injury caused by reperfusion is improved, so that the myocardial ischemia reperfusion injury is effectively prevented and treated. Furthermore, it is found that the NMRK2 can inhibit excessive activation of MST1 / p-MST1 in a Hippo pathway and promote YAP nuclear translocation, so that NADK expression is up-regulated, a Trx1 antioxidant system is enhanced, and a new 'NMRK2-YAP-NADK-Trx1 antioxidant signal pathway' is formed.

The invention belongs to the technical field of medicine preparation, and particularly relates to application of DHGC in preparation of a medicine for treating acute kidney injury ferroptosis mediated by an SIRT3 / NRF2 axis. Experiments prove that DHGC can activate SIRT3 in a targeted manner, up-regulate the expression level of SIRT3, promote NRF2 deacetylation and drive NRF2 nuclear translocation, and further up-regulate the expression level of GPX4, so that the effect of resisting ferroptosis caused by acute kidney injury is achieved.

This invention belongs to the field of biopharmaceutical technology, and specifically relates to the application of D724-0491 in the preparation of products for the prevention and treatment of breast cancer. D724-0491 inhibits the binding of HBXIP and KEAP1, reduces the level of NRF2 nuclear translocation, thereby inducing oxidative stress in tumor cells and promoting cancer cell death. It is a novel targeted therapy drug for breast cancer, improving the prognostic survival rate of breast cancer patients.

This invention proposes the application of psoralen as an Nrf2 agonist in drug preparation. This invention is the first to discover that psoralen is a specific Nrf2 agonist. Psoralen can directly target and bind to the Nrf2 protein, improving its stability, promoting its phosphorylation and nuclear translocation, thereby activating the Nrf2 signaling pathway, upregulating the expression of downstream antioxidant, anti-inflammatory, and anti-ferroptosis-related proteins, and achieving cell protection and tissue repair functions.

The application relates to the technical field of biological medicine, and provides an anti-GPC3 full humanization single-domain antibody and application thereof. The application uses phage display technology to obtain one anti-human GPC3 specificity full humanization monoclonal single-domain antibody through antibody screening by targeting human GPC3 protein. The obtained single-domain antibody can be specifically combined with human GPC3, and can effectively inhibit the nuclear translocation of YAP, provides an effective alternative antibody drug for GPC3-targeted HCC treatment, and has a potential clinical application prospect.

The invention relates to application of lentinan in preparation of a medicine for enhancing Kukuzhou cell immune function, and belongs to the technical field of immunopharmacology. The invention discloses a mechanism and application of lentinan LNT (Lentinan) based on a TLR2 (Toll-Liver Receptor 2) signal channel for enhancing the immune function of liver cumness cells and promoting lysosome maturation. By constructing an LNT fluorescence labeling system, a Kuptake cell in-vivo tracing model and a TLR2 function intervention model, it is proved that LNT can be directly combined with TLR2 and activate a TLR2 / MyD88 / NF-kappa B signal axis, and therefore the phagocytosis and immune response capacity of Kuptake cells is enhanced. Meanwhile, TLR2 signal-induced reactive oxygen species (ROS) up-regulation can promote TFEB dephosphorylation and nuclear translocation, lysosome maturation is driven, and degradation metabolism of LNT is accelerated. The invention provides a TLR2-based immune enhancement mechanism of the LNT, and provides a theoretical basis and an application basis for developing immunomodulatory targeted drugs.

The invention discloses an application of a P4HA1 inhibitor in preparation of a medicine for treating congenital megacolon-related enterocolitis, deeply clarifies an immune metabolic axis of 'P4HA1-hydroxyproline-eIF5A-IRF4-IL17', and discloses a new mechanism that metabolite hydroxyproline regulates the activity of eIF5A and promotes nuclear translocation of IRF4 so as to enhance TH17 cell mediated inflammatory response. Therefore, a brand new perspective is provided for understanding metabolic immune regulation of intestinal inflammation. By using the P4HA1 inhibitor (such as 1, 4-DPCA), secretion of IL-17 can be effectively inhibited, intestinal inflammation injury of HAEC model mice can be remarkably relieved, and a clear pharmacodynamic basis is achieved.

T lymphocytes play a key role in the immune response and their functions are intimately linked to metabolic programs. During immune responses, T cells undergo a metabolic reprogramming notably characterized by an increased aerobic glycolysis. Using a quantitative phosphoproteomic approach, the inventors have identified a new transcription factor called Foxk1 as being highly phosphorylated in T cells upon T Cell Receptor (TCR) engagement. The results also indicate that Foxk1 phosphorylation and nuclear translocation is dependent of the AKT-mTOR kinase activities. Using T-cell specific Foxk1 deficient mice (Foxk1- / -), we demonstrated that Foxk1 is required for full T cell activation. Foxk1-deficient T cells exhibited reduced proliferation and cytokine secretion following TCR stimulation. Furthermore, T cells from Foxk1- / - mice were less prone to acquire an effector like phenotype than wild-type cells when challenged in vivo. Conversely, Foxk1 overexpression in T cells enhanced their effector functions in a TCR-dependent manner. In CD8+ T cells, this effect also results into enhanced cancer cell killing capacity in vitro, and improved tumor rejection in vivo. Altogether, these results indicated that Foxk1 is a major regulator of T cell metabolism and thus, of T cell effector functions. Thus, the present invention relates to host immune cells engineered to overexpress a Foxk1 polypeptide and their use of the treatment of cancer.

The invention relates to a PKM2-based nano glycopeptide activator and application thereof.The nano glycopeptide activator comprises three functional units, namely a PKM2 targeted activation unit R3, a self-assembly unit R2 and a response unit R1, and the chemical structure of the nano glycopeptide activator is shown in the formula (I). After administration, the nano glycopeptide activator can be enriched to a tumor site through targeting of sugar receptor transporter protein or an EPR effect; after entering tumor cells, the polypeptide is subjected to in-situ fibrosis deformation under the hydrolysis action of glycohydrolase, so that specific targeting and retention are realized; the nano-fiber with the PKM2 targeting activation unit can promote conversion of dimer PKM2 into tetramer PKM2, inhibit nucleation of PKM2, and prevent the DNA damage repair process of tumor cells.

The application belongs to the technical field of biological medicine and molecular biology, and particularly relates to application of umbilical cord blood plasma-derived extracellular vesicles and related bioactive molecules thereof in treatment of Alzheimer's disease. Specifically, the application isolates extracellular vesicles (UCBP-sEVs) from umbilical cord blood plasma, which has the effect of improving Alzheimer's disease. Further research finds that high enrichment of miR-16-2-3p therein is a key molecule for mediating treatment of Alzheimer's disease. miR-16-2-3p targets and inhibits expression of ROCK2, reduces phosphorylation level of TFEB and promotes nuclear translocation of the same, activates microglial autophagy-lysosome pathway, and thus promotes phagocytosis and degradation of intracerebral beta amyloid, and therefore has good practical application value.

The invention relates to the technical field of biological medicines, and particularly discloses a nanocapsule SMCPM and application thereof in medicines for treating or preventing osteosarcoma and pulmonary metastasis. The SMCPM is composed of a photosensitizer Ce6 carried by mesoporous silicon oxide-manganese oxide particles, an NRF2 inhibitor ML385 and an OS targeting peptide PT-7. Experiments prove that the SMCPM is high in penetrating power and strong in cell killing effect; by down-regulating NRF2 expression and reversing nuclear translocation, a biochemical inhibitory microenvironment can be effectively repaired, the tolerance of cells to active oxygen and epithelial-mesenchymal transition activated and induced by a NOTCH1 signal axis are remarkably reduced, the oxidative stress level of the cells is enhanced, and PIT-induced immunogenic cell death is promoted; the released Mn < 2 + > and double-stranded DNA can regulate and control an immunosuppressive microenvironment by activating an STING pathway in cells, thereby inhibiting the growth of osteosarcoma and preventing lung metastasis.

The invention discloses application of a targeted Nup85 inhibitor in preparation of a medicine for preventing or treating hepatocellular carcinoma, and relates to the technical field of biological medicine and tumor immunotherapy. The invention provides an application of a targeted Nup85 inhibitor in preparation of a medicine for preventing or treating hepatocellular carcinoma. The inhibitor prevents and / or treats hepatocellular carcinoma by enhancing CD8 + T cell functions, enhancement of the CD8 + T cell functions is realized by regulating STAT1 / CCL5 / CXCL10 pathways, and Nup85 reduces expression of CCL5 and CXCL10 by inhibiting nuclear translocation of phosphorylated STAT1, so that infiltration and activation of CD8 + T cells are inhibited. The invention discloses an immune escape mechanism that Nup85 inhibits CD8 + T cell infiltration by inhibiting p-STAT1 nuclear translocation and down-regulating CCL5 / CXCL10 expression in liver cancer for the first time, provides a new liver cancer immunotherapy target, and broadens the application of nucleopore protein in tumor immunotherapy; the target Nup85 inhibitor can be obtained through a conventional means, a new clinical application direction of the target Nup85 inhibitor is defined, and the target Nup85 inhibitor has good clinical transformation and development prospects.

The invention discloses a composition for improving skin inflammation as well as application and a production method of the composition. The composition is prepared from the following components in parts by weight: 2 to 6 parts of curcumin monocarbonyl analogue cyclodextrin inclusion compound and 0.3 to 0.5 part of allantoin. The curcumin monocarbonyl analogue cyclodextrin inclusion compound is prepared from the following components in parts by weight: 0.5 to 1.5 parts of curcumin monocarbonyl analogue and 98.5 to 99.5 parts of beta-cyclodextrin, and the composition is applied as a skin care product. Aiming at skin inflammation caused by chronic symptoms, NF-kappa B nuclear translocation is blocked, multi-target anti-inflammation is achieved, and the effect is better directly aiming at core pathogenic genes. The allantoin increases the dissolution and absorption of the curcumin monocarbonyl analogue cyclodextrin inclusion compound, promotes the hydration of cuticle and reduces the irritation to the skin; the use effect is milder, and the composition is more suitable for non-invasive dermatitis.

Non-viral gene therapy treatments have a number of advantages over viral vectors including typical non-antigenicity, low manufacturing cost, simplicity, and efficiency of delivering genetic cargo into the cytoplasm. The potency of non-viral gene therapy systems can be enhanced by providing them with means to more efficiently transport the delivered DNA from the cytoplasm to the nucleus. Provided herein, at least in part, are means of enhancing potency of non-viral gene therapies by including novel nuclear translocation enhancing sequences and compositions that can result in optimized nuclear translocation as well as related compositions and methods.

The invention discloses a probe set. The probe set comprises a first fusion protein and a second fusion protein, wherein the first fusion protein comprises a nuclear localization sequence and a first protein molecule, and the nuclear localization sequence is connected with the first protein molecule; the second fusion protein comprises a TFEB protein and a second protein molecule, the TFEB protein is connected with the second protein molecule, the second protein molecule is used for being combined with the first protein molecule, and a detectable signal is generated after the first protein molecule and the second protein molecule are combined. The probe set can rapidly, accurately and sensitively detect the TFEB nuclear transfer condition, can be used for high-throughput screening of TFEB regulation and control drugs, and reduces the drug screening cost.

The invention provides a rice bran protein source Keap1 inhibitory peptide as well as a preparation method and application thereof, and belongs to the technical field of biology. The invention provides a Keap1 inhibitory peptide. The Keap1 inhibitory peptide comprises a peptide 1 (SEQ ID NO: 1) and / or a peptide 2 (SEQ ID NO: 2). The Keap1 inhibitory peptide is a natural short peptide which is separated and identified from rice bran and can be directly combined with a Keap1 protein, can be used as a direct inhibitor of the Keap1 protein, and can be competitively combined with a Kelch structural domain of Keap1 to block interaction between Keap1 and Nrf2 and promote Nrf2 nuclear translocation and expression of a downstream antioxidant gene, so that endogenous antioxidant defense of cells is enhanced, and the Keap1 inhibitory peptide can be used for preparing a Keap1 inhibitor. The method can be widely applied to anti-oxidation product preparations.

The invention discloses a nano preparation for blocking malignant crosstalk of mechanical and biochemical signals of a lung. The preparation is composed of lipid nanoparticles composed of phospholipid, cholesterol and DSPE-PEG2K-NH2, the surfaces of the lipid nanoparticles are grafted with L-arginine and tannic acid, the two drugs are cooperatively loaded, and double intervention on mechanical and biochemical signal channels is achieved. Tannic acid modification can remove active oxygen and enhance lung targeting, and L-arginine is helpful to penetrate through a compact extracellular matrix and promote delivery of drugs to the deep part of pulmonary alveoli. On one hand, by promoting phenotype reversion of myofibroblast-like endothelial cells to endothelium, endothelial-mesenchymal transformation is reduced, and fibrosis progress is inhibited; on the other hand, nuclear translocation of mechanical conduction factors is blocked, and mechanical signal channels related to fibrosis are intervened. The nano preparation can effectively reverse malignant crosstalk of mechanical and biochemical signals in fibrotic lung tissues, and provides an innovative and efficient treatment strategy for pulmonary fibrosis.

Compounds having general formula I, a method for preparing same, a pharmaceutical composition thereof, and use thereof are provided. Specifically, a compound having a structure represented by general formula I, and a racemate, an R-isomer, an S-isomer and a pharmaceutically acceptable salt thereof, or a mixture thereof are provided. The compound promotes transcription factor EB (TFEB) nuclear translocation and lysosome generation, and can be used for preventing, treating, or assisting in treating various diseases related to lysosome dysfunction and biosynthesis insufficiency, especially neurodegenerative diseases caused by the accumulation of intracerebral pathological proteins (e.g., β-amyloid protein and α-synuclein), such as Alzheimer's disease (AD) and Parkinson's disease (PD).

This invention relates to the field of biomedical technology, and more particularly to the application of an isoflavone compound, specifically Corylifol A, in the preparation of drugs for the prevention and / or treatment of inflammatory diseases. When used to prepare drugs for the prevention and / or treatment of inflammatory diseases, this isoflavone compound can directly bind to the IκBα protein and specifically inhibit its phosphorylation, thereby blocking the phosphorylation and nuclear translocation of the NF-κB p65 subunit, ultimately inhibiting the overactivation of the NF-κB signaling pathway. Furthermore, the isoflavone compound can significantly reduce the mortality rate of lipopolysaccharide-induced septicemia in mice, inhibit the levels of inflammatory factors in serum and lung tissue, and effectively alleviate LPS-induced acute lung injury in mice. Simultaneously, when the isoflavone compound is controlled within an effective concentration range, it exhibits no significant cytotoxicity to mouse peritoneal macrophages and can significantly inhibit the production and release of lipopolysaccharide-induced inflammatory factors IL-1β, TNF-α, and IL-6.

The invention provides application of a CD5-targeting reagent in the aspects of reducing the drug resistance of tumor cells and improving the anti-tumor curative effect of drugs, and clarifies for the first time that CD5 molecules can promote high expression and cell nucleus displacement of transcription factors FOXO3a and FOXO4 in a forkhead cassette O signal channel; therefore, expression increase of the ABC drug-resistant protein family in diffuse large B-cell lymphoma tumor cells is mediated, and drug resistance of tumor cells to various chemotherapeutic drugs is promoted. Further, it is found that the celecoxib can significantly inhibit expression of CD5 molecule mediated ABC drug-resistant protein in B-cell lymphoma cells, then the celecoxib and chemotherapeutic drugs are combined for application, the killing effect of traditional chemotherapeutic drugs on diffuse large B-cell lymphoma tumor cells is significantly enhanced, and the chemotherapeutic drug resistance of diffuse large B-cell lymphoma is overcome. The anti-drug-resistant tumor strategy can overcome the problems of low treatment response rate and poor prognosis of the CD5-positive diffuse large B-cell lymphoma to the existing chemotherapy regimen due to multidrug resistance, and significantly improves the anti-tumor treatment effect.

The invention belongs to the technical field of genes and biomedicine, and particularly relates to a marker serving as a head and neck squamous cell carcinoma treatment target and application, the marker is an aerobic glycolysis key enzyme PFKP, and the aerobic glycolysis key enzyme PFKP promotes in-vivo glycolysis metabolism and head and neck squamous cell carcinoma progress through AMOTL1 / YAP / Hippo. The key enzyme PFKP for aerobic glycolysis is a key prognosis factor of the HNSCC, promotes aerobic glycolysis and epithelial-mesenchymal transition of the HNSCC, directly interacts with AMOTL1, inhibits ubiquitination degradation of the AMOTL1, promotes EMT and aerobic glycolysis of the HNSCC by depending on the AMOTL1, the PFKP targets the AMOTL1 to promote YAP nuclear translocation in the HNSCC, PFKP / AMOTL1 depends on the nuclear translocation of YAP to enhance the aerobic glycolysis and tumor progression of the HNSCC, and the HNSCC has the advantages that the key enzyme PFKP can be used for inhibiting the tumor progression of the HNSCC. The enhanced PFKP promotes the progress of the HNSCC in vivo through the AMOTL1 / YAP (AMOTL1 / YAP).

Targeting the ability of T cells to enhance aerobic glycolysis upon TCR stimulation or glucose supplementation represents an attractive strategy for the treatment of autoimmune diseases. Using a quantitative phosphoproteomic approach, the inventors have identified a new transcription factor called Foxk1 as being highly phosphorylated in T cells upon T Cell Receptor (TCR) engagement. The results also indicate that Foxk1 phosphorylation and nuclear translocation is dependent of the AKT-mTOR kinase activities. Using T-cell specific Foxk1 deficient mice (Foxk1- / -), the inventors demonstrated that Foxk1 is required for full T cell activation. Foxk1-deficient T cells exhibited reduced proliferation and cytokine secretion following TCR stimulation. Furthermore, T cells from Foxk1- / - mice were less prone to acquire an effector like phenotype than wild-type cells when challenged in vivo. Altogether, these results indicated that targeting can be envisioned to reduce auto-immune reactions. Thus, the present invention relates to the use of Foxk1 inhibitors for the treatment of inflammatory autoimmune diseases.

This invention provides the application of the LHPP gene in liver cancer immunotherapy and liver cancer immunotherapy drugs. Reagents that promote LHPP gene expression can be used to prepare liver cancer immunotherapy drugs. This invention also provides an mRNA nanomedicine, which is prepared by the following method: [The invention then describes a process involving Meo-PEG-Dlink]. m A PLGA solution, an aqueous solution of LHPP gene mRNA, and a cationic liposome solution were mixed and added dropwise to water under stirring to obtain a nanosolution. The nanosolution was then transferred to an ultrafiltration membrane and centrifuged. This invention is the first to discover that LHPP can participate in the immunotherapy of liver cancer and is associated with the survival prognosis of liver cancer. LHPP enhances STAT1 nuclear translocation by affecting the expression of autophagy-regulated IFNβ, thereby promoting the expression of T cell-related chemokines secreted by liver cancer cells, and ultimately promoting CD8+ expression. + T cell infiltration. Therefore, the LHPP gene can serve as a novel target for immunotherapy of liver cancer. The mRNA nanomedicine described has advantages such as long circulation time in the blood, high accumulation in tumors, rapid mRNA release, and low cost.

The invention provides an application of a biliverdin reductase inhibitor in preparation of a medicine for treating hemorrhagic stroke, relates to the technical field of biological medicines, and discloses that biliverdin reductase generates pathological nuclear translocation in the hemorrhagic stroke, and a lipid peroxidation pathway is activated through co-localization of the biliverdin reductase and a lipid metabolism key enzyme ACSL4, so that the biliverdin reductase inhibitor can be used for treating the hemorrhagic stroke. The nerve cell ferroptosis is driven; the biliverdin reductase is used as a novel treatment target, and the inhibitor can effectively relieve iron overload, improve lipid peroxidation, recover GPX4 expression and reduce nerve cell ferroptosis by specifically blocking biliverdin reductase expression or nuclear translocation on the premise of not remarkably interfering the physiological cytoplasm antioxidant function of biliverdin reductase. And finally, the neurological impairment of an animal model is remarkably improved, and the method has the clinical safety advantages of mechanism novelty, curative effect verifiability, targeting accuracy and avoidance of high bilirubin toxicity risk.

The invention discloses a traditional Chinese medicine composition for preventing hair loss and growing hair by inhibiting DHT receptor expression and a preparation method of the traditional Chinese medicine composition, and belongs to the technical field of hair growing and caring products, the traditional Chinese medicine composition comprises a nano compound, and the nano compound is formed by noni fruit extract FEA-3 and molybdate through coordination driven self-assembly, the morinda citrifolia extract FEA-3 serves as a reducing agent and a stabilizing agent of molybdate, molybdenum-based nano-particles with the particle size of 50-1200 nm are formed through induction, the morinda citrifolia extract FEA-3 is rich in polyphenol structures and can be specifically combined with androgen receptors on the surfaces of hair follicle cells, and the molybdenum-based nano-particles are used for inhibiting combination of male hormone receptor nuclear translocation and DHT in the cells, so that the morinda citrifolia extract FEA-3 can be used for preparing the hair follicle. A downstream signal channel of a male hormone receptor is blocked, so that hair follicle microminiaturization is inhibited, and hair growth is promoted. The traditional Chinese medicine composition provided by the invention realizes synchronization of androgen receptor protein degradation and androgen receptor gene silencing in hair follicle cells.

This invention discloses a circular RNA, circTP63-N, and its applications. This invention discovers a novel circular RNA, circTP63-N, expressed at low levels in nasopharyngeal carcinoma. By directly binding to the HSP90AB1 protein, it promotes the binding of LATS1 / 2 and YAP1 proteins, causing YAP1 phosphorylation and ubiquitination degradation, leading to reduced YAP1 nuclear translocation. This further inhibits the expression of downstream extracellular matrix-related genes INHBA and MMP3, as well as the cell cycle-related gene CCNE2, ultimately suppressing the proliferation, invasion, and migration of nasopharyngeal carcinoma. The discovery of this circular RNA provides a new approach for the diagnosis and treatment of nasopharyngeal carcinoma and has broad application prospects.

The invention discloses application of andrographolide and a pharmaceutical composition thereof in preparation of a medicine for preventing and / or treating lung cancer, particularly lung metastatic tumor, and belongs to the technical field of medicine. In-vivo and in-vitro experiments of a system prove that andrographolide can inhibit activation of a nuclear factor kappa B (NF-kappa B) signal channel by down-regulating expression of glycogen synthase kinase 3beta (GSK3beta), and particularly, phosphorylation and nuclear translocation processes of an NF-kappa B p65 subunit Ser536 site are inhibited. According to the effect, transcription and expression of downstream target gene chemotactic factors CCL2 and CXCL1 are effectively reduced, finally, infiltration of tumor-related macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) in tumor tissue is remarkably reduced, aggregation of anti-tumor immune cells such as CD8 + T cells is promoted, an immunosuppressive microenvironment is reversed into an immune activation state, and the immunosuppressive activity of tumor cells is improved. And lung cancer metastasis is inhibited from the source. The invention provides a brand new candidate drug and a clear action mechanism for clinical prevention and treatment of lung cancer metastasis, and has a good development prospect.

The object of the present invention is to provide a novel composition for inhibiting the nuclear translocation of NFATc1 and NFATc2 for anti-allergic purposes. [Solution] The NFATc1 and NFATc2 nuclear translocation inhibitory composition according to the present invention contains an aqueous extract of Terminalia bellirica fruit as an active ingredient. The term "composition" as used herein includes preparations such as liquid foods, supplements and food additives, food and beverages (excluding plants and animals themselves), food and beverage compositions (including processed food and beverages), pharmaceutical compositions, and other substances that can be ingested by animals (including humans).