{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Jie Xu"],"species":["Homo Sapiens"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0010033000"],"submitter_email":["jie_xu@fudan.edu.cn"],"submitter_affiliation":["Fudan University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"pubmed_abstract":["T cells within the tumor microenvironment frequently exhibit dysfunctional characteristics that compromise their ability to elicit both innate and therapeutic-induced immune responses. Regulators of immune dysfunction represent therapeutic targets to activate antitumor immunity. In this study, we identified semaphorin 3G (SEMA3G) as a key regulator of immune responses in cancer. SEMA3G was widely upregulated in diverse human cancers, and its expression was positively correlated with tumor progression. SEMA3G acted as a ligand that inhibited the activation and functionality of T cells. A comprehensive receptor screening approach demonstrated that SEMA3G exhibited a significantly stronger affinity for neuropilin (NRP) 1 than for NRP2. Furthermore, SEMA3G primarily impeded T-cell functions via NRP1. Disruption of SEMA3G using CRISPR/Cas9 technology or blockade with a neutralizing antibody effectively restored the cytotoxicity of CD8+ T cells and inhibited the growth of tumors in vivo. This research underscores the role of SEMA3G in T-cell dysfunction within tumors and proposes targeting SEMA3G as a cancer immunotherapeutic strategy. Significance: SEMA3G binding to NRP1 suppresses cytotoxic T-cell activity to induce an immunosuppressive tumor microenvironment, positioning SEMA3G as a promising therapeutic target for improving cancer immunotherapy."],"pubmed_title":["SEMA3G-NRP1 Signaling Functions as an Immune Checkpoint That Enables Tumor Immune Evasion by Impairing T-cell Cytotoxicity."],"pubmed_authors":["Chi Hao H, Deng Shouyan S, Xu Ke K, Zhang Yibo Y, Song Teng T, Yu Jianghong J, Wang Yiting Y, Liu Jiayang J, Zhang Yuan Y, Shi Jiawei J, Wang Yungang Y, Xu Jie J"],"name_synonyms":["Mass Spectrum Analysis, BPBS, treatment, Therapy, Mass Spectrum, absence of, Painful Bladder Syndrome, with urinary tract Abnormality and cryptorchidism, Peripheral Blood, whole blood, BZRP, Analyses, DBI, Blood, Spectrometry, IBP, pk18, Spectrum Analyses, abdominal muscles, mDRC, Spectrum Analysis, MBR, Treatments, Reticuloendothelial System, PBS, Spectroscopy, PBR, disease management., MS, Painful bladder syndrome, PKBS, Therapeutic, PBMC, PBMCs, Mass, Therapies, PTBR, Treatment, Analysis, Bladder pain syndrome, eagle-Barrett syndrome, Mass Spectrum Analyses, Mass Spectroscopy, Bladder Pain Syndrome"],"pubmed_abstract_synonyms":["Class 3 Semaphorins, l(1)d norm-12, Class 2 Semaphorins, Class 4 Semaphorins, CRISPR Locus, CRISPR Loci, Class 5 Semaphorins, Unspecified disorder of immune mechanism, Class 1 Semaphorins, EG:17A9.1, Clustered Regularly Interspaced Short Palindromic Repeat, Activity, C530029I03, BR_C, Laboratory, Feature, CRISPR Spacer, Semaphorin V, postnatal development, 2Bc, growth and development, T-Lymphocyte, killer T lymphocyte, Tumor, BR-C, ALS12, Other specified disorders of the immune mechanism (disorder), Semaphorin 1, unspecified, Other specified disorders involving the immune mechanism, Semaphorin 5, l(1)2Bad, A18, br-C, T Lymphocyte, Semaphorin 4, Semaphorin 3, l(1)2Bab, Roles, Semaphorin 2, br-Z1, Semaphorin 7, Semaphorin 6, br-Z3, symptoms, PP1, Concepts, PP2, Research Activity, Tumor Microenvironments, BR-c, Br-C, l(1)dn1, immature T cell, Laboratory Research, IKKg, Arrays, KEY, Key, Priorities, Br-Z4, rbp, DEFIC CELL IMMUNITY NOS, Immune Processes, Immune Responses, Deficiency of cell-mediated immunity, Man (Taxonomy), killer T-lymphocyte, Autoimmune disease, l(1)G0318, de12, Elements, T-Cells, [X]Disorder involving the immune mechanism, BR, Immune System and Related Disorders, l(1)n34, T, BrC-Z1, killer T-cell, cytotoxic T-cell, Br-C-Z3, CRISPRs, T Cells, Immune, malignant neoplasm, Role Concepts, Therapies, Br, BRC-Z2, BRC-Z3, BRC-Z1, Malignancies, BRC-Z4, Research Priority, Class 7 Semaphorins, Class 6 Semaphorins, Thymus Dependent Lymphocytes, CG11491, Semaphorin-V, cytolytic T-lymphocyte, Tumors, rdp, Cancer Microenvironments, rds, Therapy, NRP1, screening, NRP2, Semaphorin-7, CRISPR Spacer Sequences, CRISPR Clusters, Ligand, HIP7, Process, Modern, Arts, BR-C Z1, l(1)d.norm.1, Aptitudes, Np2, Research Priorities, CRISPR Arrays, Semaphorin-2, l(1)npr-1, CRISPR-Cas, Clusters, Semaphorin-1, Semaphorin-6, uq, Semaphorin-5, Semaphorin-4, l(1)npr1, Semaphorin-3, Ability, DmIKKgamma, CRISPR Element, Immunodeficiency and Immunosuppression Disorders, Benign, Screenings, Role Concept, T-Cell, dIKK, NP1, Kenny, Role, NP2, nrp1, regulator, CD304, activation, VEGF165R, Semaphorin, GLC1E, Npn1, Research and Development, NP-1, NPN2, Npn2, immune system disorder, T-cell, Industrial, Element, Industrial Arts, growth pattern, non-developmental growth, p32, Thymus-Dependent, IKK-gamma, signs, Benign Neoplasms, npr-1, T-lymphocyte, Features, IDH3GL, Treatments, cytotoxic T-lymphocyte, human, Thymus-Dependent Lymphocyte, Malignant Neoplasms, Activities, cytolytic T-cell, immune dysfunction, 1110048P06Rik, T cell, DmelCG16910, Cluster, Cells, Spacers, HYPL, NAP1, npr, l(1)pp-2, l(1)pp-1, T Cell, Spacer Sequences, Semaphorins, IMMUNE MECHANISM DIS NEC, other neoplasm, Class V Semaphorins, Disorder of the immune mechanism NOS, NPN-1, F6A14.10, CRISPR-Cas Loci, VEGF165R2, Thymus-Dependent Lymphocytes, human being, Neuropilin, Microenvironment, NRP, Nrp, Neoplasms, l(1)G0018, DmelCG11491, Npn-2, AUTOIMMUNE DISEASE NEC, cytotoxic T cell, Benign Neoplasm, l(1)ts144, F6A14_10, l(1)2Ba, l(1)2Bb, CRISPR Array, Z1, l(1)2Bc, Z2, Z3, Z4, Malignant, dIKK-gamma, unspecified (disorder), Human, CG11511, Np-2, Antibody, EG:25D2.1, CG11514, non-replicating persistence, Homo sapiens, Cancer Microenvironment, DmIKK-gamma, nrp, Br-C Z2, Mass, l(1)ts132, Screening, l(1)ts376, IMMUNE MECHANISM DIS NOS, Neutralizing Antibody, dmIKKgamma, IKK[[gamma]], MAL, Man, CRISPR Spacers, l(1)ESHS5, study, Other deficiency of cell-mediated immunity, Malignancy, Research, Disorders involving the immune mechanism, ligand, nprl, dysfunction, Treatments., CRISPR Spacer Sequence, immune disorder, CRISPR Sequences, CRISPR Cluster, Neoplasias, CRISPR, Abilities, CRISPR-Cas Locus, l(1)G0042, l(1)G0284, PRO2714, Immune Response, IKK, l(1)2Bd, mature T cell, Loci, Class 1, Class 3, npr1, Class 2, Sema 1, Class 5, l(1)PP1, l(1)pp1, Characteristics, Class 4, Development and Research, Class 7, Neutralizing, Class 6, l(1)pp2, Neutralizing Antibodies, Immune Process, T Lymphocytes, Lymphocyte, Spacer Sequence, Cancer, EG:123F11.1, CRISPR Sequence, findings, Malignant Neoplasm, NAP1-related protein 2, NAP1-related protein 1, not elsewhere classified, killer T cell, NAP1L, Leu2, ecs, BrZ3, Class V, l(1)G0284a, Cell, disease or disorder of immune system, Concept, Sequences, development, IKKgamma, TFIIIA-INTP, Priority, Characteristic, MT, o.c.c., Mass Screenings, Sequence, CRISPR Elements, Research Activities, Neoplasm, cytotoxic T lymphocyte, Spacer, Disorder of the immune mechanism NOS (disorder), T lymphocyte, immune system disease or disorder, F1M20_24, primary cancer, FIP2, Exhibit, IMMUNDEF T-CELL DEF NOS, Dmikkgamma, l(1)ts358, postnatal growth, Talents, Lymphocytes, BDCA4, Cancers, pathophysiology, disease of immune system, CG16910, malignant tumor, Locus, disorder of immune system, autoimmune diseases, immune disease, 2B5, Therapeutic, Talent, l(1)G0401, Modern Man, 4930441O07Rik, F1M20.24, Response, Array, Other specified disorders of the immune mechanism, CRISPR Cas Loci, BRC, Treatment, CD8, Microenvironments, growth, CTL, General activity, Neoplasia, Immunodeficiency with predominant T-cell defect"],"pubmed_title_synonyms":["l(1)d norm-12, NPN-1, Thymus-Dependent Lymphocytes, EG:17A9.1, C530029I03, BR_C, Nrp, NRP, l(1)G0018, DmelCG11491, 2Bc, l(1)ts144, l(1)2Ba, l(1)2Bb, Z1, l(1)2Bc, T-Lymphocyte, Z2, BR-C, Z3, Tumor, Z4, CG11511, EG:25D2.1, CG11514, l(1)2Bad, A18, br-C, Immune Evasions, T Lymphocyte, l(1)2Bab, br-Z1, nrp, Br-C Z2, br-Z3, PP1, l(1)ts132, l(1)ts376, PP2, Immune Evasion, BR-c, Br-C, l(1)dn1, immature T cell, l(1)ESHS5, Br-Z4, rbp, Tumor Immune Evasions, l(1)G0318, de12, T-Cells, nprl, BR, l(1)n34, BrC-Z1, T, Br-C-Z3, T Cells, l(1)G0042, l(1)G0284, l(1)2Bd, mature T cell, Br, BRC-Z2, BRC-Z3, npr1, Evasions, BRC-Z1, l(1)PP1, l(1)pp1, BRC-Z4, l(1)pp2, T Lymphocytes, CG11491, Thymus Dependent Lymphocytes, Lymphocyte, single organism signaling, rdp, rds, NRP1, EG:123F11.1, Immune Escape, Tumor Immune, NAP1-related protein 1, BR-C Z1, l(1)d.norm.1, Evasion, ecs, BrZ3, l(1)npr-1, l(1)G0284a, uq, Cell, l(1)npr1, Tumor Immune Evasion, o.c.c., T-Cell, NP1, nrp1, CD304, T lymphocyte, VEGF165R, Npn1, F1M20_24, NP-1, Thymus-Dependent Lymphocyte., T-cell, l(1)ts358, Thymus-Dependent, BDCA4, Lymphocytes, npr-1, T-lymphocyte, IDH3GL, Tumor Immune Escape, 2B5, T cell, signalling process, l(1)G0401, Cells, F1M20.24, npr, l(1)pp-2, BRC, l(1)pp-1, T Cell"],"description_synonyms":["Class 3 Semaphorins, glicoproteinas, Networks, Class 2 Semaphorins, Class 4 Semaphorins, Class 5 Semaphorins, O-Glycosylated, Class 1 Semaphorins, Kinship, single-organism developmental process, Product, Semaphorin V, postnatal development, growth and development, Tumor, Cell Interactions, dmTAF[[II]]230, Semaphorin 1, Glycoprotein, Semaphorin 5, Communications, Semaphorin 4, Semaphorin 3, glycoproteins, Roles, Semaphorin 2, Biological, Semaphorin 7, Semaphorin 6, Concepts, Life Cycle, Cell-to-Cell, Biological Product, glycoproteine, C-Glycosylated Proteins, Family Life Cycle, glicoproteina, Glykoprotein, Immune Processes, N-Glycosylated, Immune Responses, Kinship Network, Biologic Drugs, TFIID TAF250, cel, Natural, Cell to Cell Interaction, membrane region, Biological Drugs, Communication, Immune, Biological Medicine, Role Concepts, Medicine, Malignancies, Medicines, Family Life Cycles, Glycosylated Protein, Class 7 Semaphorins, Class 6 Semaphorins, Biologic Drug, Semaphorin-V, Neoglycoproteins, Tumors, a glycoprotein, Semaphorin-7, dTAF[[II]]230, Process, Biologic Products, TAF200, integral to membrane, Semaphorin-2, Semaphorin-1, TAFII-250, TAF250/230, Semaphorin-6, Semaphorin-5, Semaphorin-4, Semaphorin-3, TAFII250, Interaction, Role Concept, Benign, Biopharmaceuticals, Role, Biologic Product, Filiation, Semaphorin, Cell Communications, growth pattern, Biological Medicines, non-developmental growth, Glycosylated, Biological Drug, frequency., Benign Neoplasms, Biologics, CG17603, TAF[[II]], surveillance, morbidity, Malignant Neoplasms, Life Cycles, Taf250, SR3-5, microarray, Semaphorins, other neoplasm, Class V Semaphorins, TAF230, d230, Family Member, C-Glycosylated, Biologic Pharmaceuticals, Neoplasms, Benign Neoplasm, dTAFII250, Network, EfW1, Malignant, dmTAF1, Taf230, integral component of membrane, Cell-to-Cell Interactions, TAF250, Biologicals, Drugs, study, Taf200, dTAF[[II]]250, Cell Interaction, Malignancy, Research, occurrence, cell, glycoproteines, Natural Product, prevalence, Cell-to-Cell Interaction, Taf1p, O-Glycosylated Proteins, Neoplasias, dTAF250, Immune Response, Class 1, region of membrane, Class 3, Class 2, Sema 1, immune cell activation, Class 5, Class 4, Class 7, Kinship Networks, Class 6, TAF, Family, Immune Process, Biologic, incidence, Glykoproteine, Pharmaceuticals, Cancer, Products, TAF[[II]]250, Malignant Neoplasm, Family Research, Biologic Medicines, Proteins, l(3)84Ab, Class V, BG:DS00004.13, leucocyte activation, Cell, dTAF230, Concept, Family Members, development, p230, Protein, Glycosylated Proteins, Biopharmaceutical, whole membrane, Neoplasm, TAF[[II]]250/230, TFIID, outbreaks, Taf[[II]]250, transmembrane, TAF[[II]]230, N-Glycosylated Proteins, postnatal growth, TAF[II]250, Cancers, endemics, Drug, DmelCG17603, Families, Response, Natural Products, epidemics, Relatives, growth, Interactions, Neoplasia, TAF1"],"additional_accession":[]},"is_claimable":false,"name":"Mass spectrometry data of PBMCs after PBS/SEMA3G treatment","description":"The semaphorins encompass a substantial family of secreted and transmembrane glycoproteins, originally recognized as pivotal factors in guiding axonal growth during the development of neural circuitry. Recent studies have uncovered diverse functions of semaphorins in a wide array of immune responses, encompassing immune cell activation, differentiation, migration, and cell-cell interactions, contingent upon their transmembrane receptors and co-receptors within specific biological contexts. However, a comprehensive investigation exploring the role, mechanism, and the interplay between SEMA3G and tumor immune surveillance remains elusive.","dates":{"publication":"Fri Oct 25 00:00:00 GMT+01:00 2024"},"accession":"PXD057174","cross_references":{"TAXONOMY":["9606"],"pubmed":["39652581"]}}