BACH1 as a potential target for immunotherapy in glioblastomas
•We confirmed that BACH1 as an independent prognostic indicator was enriched in glioblastomas.•BACH1 was strongly related to immune responses in glioblastoma, especially M0 and M2 tumour-associated macrophages mediated immune response.•We constructed polygenic risk scoring model and compound nomogra...
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| Veröffentlicht in: | International immunopharmacology 2022-02, Vol.103, p.108451-108451, Article 108451 |
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| creator | Yuan, Feng Cong, Zixiang Cai, Xiangming Zhu, Junhao Yuan, Lei Wang, Yingshuai Tang, Chao Ma, Chiyuan |
| description | •We confirmed that BACH1 as an independent prognostic indicator was enriched in glioblastomas.•BACH1 was strongly related to immune responses in glioblastoma, especially M0 and M2 tumour-associated macrophages mediated immune response.•We constructed polygenic risk scoring model and compound nomogram model based on BACH1, which might provide a reliable prognosis assessment tool.
Glioblastoma (GBM, WHO grade 4) is a highly heterogeneous and aggressive primary malignant brain tumor. BTB domain and CNC homology 1 (BACH1) is a transcription factor, and it plays an essential role in regulating tumor metastasis, tumor metabolism, and tumor stem cell self-renewal. However, its role in glioma is still unclear. In this research, we confirmed that BACH1 as an independent prognostic indicator was enriched in GBMs. BACH1 was strongly correlated with immune responses in GBMs, especially the M0 and M2 tumor-associated macrophage (TAM) mediated immune responses. GBMs with high expression of BACH1 express high levels of immune checkpoints (ICs), glioma cell-derived TAM chemokines, and M2 TAM markers. Interestingly, single cell RNA-seq analysis showed that the expression level of BACH1 in TAMs was higher than that in the other cell types in GBM. Transcriptome analysis of U87-MG cells showed that compared with the BACH1-vector U87-MG group, glioma cell-derived TAM chemokines (including monocyte chemotactic protein-1 (MCP-1), granulocyte–macrophage colony-stimulating factor (GM-CSF), and EGF) and ICs (including CD276, TIM-3, LAG3, TIGIT and LGALS9) were enriched in the BACH1-overexpressing U87-MG group. In addition, we constructed a polygenic risk scoring model and compound nomogram model based on BACH1, which might provide a reliable prognosis assessment tool for clinicians and aid in treatment decision-making in the clinic. In conclusion, this research identified that BACH1 might be a potential molecular signature for survival and immunotherapy response. GBMs with high expression of BACH1 have a stronger immunosuppressive tumor microenvironment (TME). Overexpression of BACH1 can upregulate the expression of glioma cell-derived TAM chemokines and ICs in vitro. Moreover, the risk model and nomogram model based on BACH1 can provide a reliable prognosis assessment tool. Therefore, BACH1 is a promising therapeutic target for GBMs. |
| doi_str_mv | 10.1016/j.intimp.2021.108451 |
| format | Article |
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Glioblastoma (GBM, WHO grade 4) is a highly heterogeneous and aggressive primary malignant brain tumor. BTB domain and CNC homology 1 (BACH1) is a transcription factor, and it plays an essential role in regulating tumor metastasis, tumor metabolism, and tumor stem cell self-renewal. However, its role in glioma is still unclear. In this research, we confirmed that BACH1 as an independent prognostic indicator was enriched in GBMs. BACH1 was strongly correlated with immune responses in GBMs, especially the M0 and M2 tumor-associated macrophage (TAM) mediated immune responses. GBMs with high expression of BACH1 express high levels of immune checkpoints (ICs), glioma cell-derived TAM chemokines, and M2 TAM markers. Interestingly, single cell RNA-seq analysis showed that the expression level of BACH1 in TAMs was higher than that in the other cell types in GBM. Transcriptome analysis of U87-MG cells showed that compared with the BACH1-vector U87-MG group, glioma cell-derived TAM chemokines (including monocyte chemotactic protein-1 (MCP-1), granulocyte–macrophage colony-stimulating factor (GM-CSF), and EGF) and ICs (including CD276, TIM-3, LAG3, TIGIT and LGALS9) were enriched in the BACH1-overexpressing U87-MG group. In addition, we constructed a polygenic risk scoring model and compound nomogram model based on BACH1, which might provide a reliable prognosis assessment tool for clinicians and aid in treatment decision-making in the clinic. In conclusion, this research identified that BACH1 might be a potential molecular signature for survival and immunotherapy response. GBMs with high expression of BACH1 have a stronger immunosuppressive tumor microenvironment (TME). Overexpression of BACH1 can upregulate the expression of glioma cell-derived TAM chemokines and ICs in vitro. Moreover, the risk model and nomogram model based on BACH1 can provide a reliable prognosis assessment tool. Therefore, BACH1 is a promising therapeutic target for GBMs.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2021.108451</identifier><identifier>PMID: 34923423</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Basic-Leucine Zipper Transcription Factors - genetics ; Basic-Leucine Zipper Transcription Factors - metabolism ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Brain cancer ; Brain Neoplasms - diagnosis ; Brain Neoplasms - genetics ; Brain Neoplasms - metabolism ; Brain tumors ; BTB and CNC homology 1 (BACH1) ; Cell Line, Tumor ; Cell self-renewal ; Cerebrospinal fluid ; Chemokines ; Chemokines - metabolism ; Colony-stimulating factor ; Datasets as Topic ; Decision making ; Gene expression ; Gene Expression Regulation, Neoplastic ; Glioblastoma ; Glioblastoma (GBM) ; Glioblastoma - diagnosis ; Glioblastoma - genetics ; Glioblastoma - metabolism ; Glioma cells ; Granulocyte-macrophage colony-stimulating factor ; Homology ; Humans ; Immune checkpoint ; Immune response ; Immunotherapy ; Immunotherapy - methods ; Macrophage Activation ; Medical prognosis ; Metabolism ; Metastases ; Molecular Targeted Therapy ; Monocyte chemoattractant protein 1 ; Monocytes ; Nomograms ; Prognosis ; Risk ; Scoring models ; Stem cells ; Survival Analysis ; Therapeutic targets ; Transcriptome sequencing ; Transcriptomes ; Tumor microenvironment ; Tumor microenvironment (TME) ; Tumor-Associated Macrophages - physiology ; Tumors</subject><ispartof>International immunopharmacology, 2022-02, Vol.103, p.108451-108451, Article 108451</ispartof><rights>2021 Elsevier B.V.</rights><rights>Copyright © 2021 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier BV Feb 2022</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-21962a2b3919b17ccc29f980745d8fb020a1327b770e389153631041a187a0183</citedby><cites>FETCH-LOGICAL-c390t-21962a2b3919b17ccc29f980745d8fb020a1327b770e389153631041a187a0183</cites><orcidid>0000-0002-8132-9224 ; 0000-0002-1710-5955</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2021.108451$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27928,27929,45999</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34923423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Feng</creatorcontrib><creatorcontrib>Cong, Zixiang</creatorcontrib><creatorcontrib>Cai, Xiangming</creatorcontrib><creatorcontrib>Zhu, Junhao</creatorcontrib><creatorcontrib>Yuan, Lei</creatorcontrib><creatorcontrib>Wang, Yingshuai</creatorcontrib><creatorcontrib>Tang, Chao</creatorcontrib><creatorcontrib>Ma, Chiyuan</creatorcontrib><title>BACH1 as a potential target for immunotherapy in glioblastomas</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>•We confirmed that BACH1 as an independent prognostic indicator was enriched in glioblastomas.•BACH1 was strongly related to immune responses in glioblastoma, especially M0 and M2 tumour-associated macrophages mediated immune response.•We constructed polygenic risk scoring model and compound nomogram model based on BACH1, which might provide a reliable prognosis assessment tool.
Glioblastoma (GBM, WHO grade 4) is a highly heterogeneous and aggressive primary malignant brain tumor. BTB domain and CNC homology 1 (BACH1) is a transcription factor, and it plays an essential role in regulating tumor metastasis, tumor metabolism, and tumor stem cell self-renewal. However, its role in glioma is still unclear. In this research, we confirmed that BACH1 as an independent prognostic indicator was enriched in GBMs. BACH1 was strongly correlated with immune responses in GBMs, especially the M0 and M2 tumor-associated macrophage (TAM) mediated immune responses. GBMs with high expression of BACH1 express high levels of immune checkpoints (ICs), glioma cell-derived TAM chemokines, and M2 TAM markers. Interestingly, single cell RNA-seq analysis showed that the expression level of BACH1 in TAMs was higher than that in the other cell types in GBM. Transcriptome analysis of U87-MG cells showed that compared with the BACH1-vector U87-MG group, glioma cell-derived TAM chemokines (including monocyte chemotactic protein-1 (MCP-1), granulocyte–macrophage colony-stimulating factor (GM-CSF), and EGF) and ICs (including CD276, TIM-3, LAG3, TIGIT and LGALS9) were enriched in the BACH1-overexpressing U87-MG group. In addition, we constructed a polygenic risk scoring model and compound nomogram model based on BACH1, which might provide a reliable prognosis assessment tool for clinicians and aid in treatment decision-making in the clinic. In conclusion, this research identified that BACH1 might be a potential molecular signature for survival and immunotherapy response. GBMs with high expression of BACH1 have a stronger immunosuppressive tumor microenvironment (TME). Overexpression of BACH1 can upregulate the expression of glioma cell-derived TAM chemokines and ICs in vitro. Moreover, the risk model and nomogram model based on BACH1 can provide a reliable prognosis assessment tool. Therefore, BACH1 is a promising therapeutic target for GBMs.</description><subject>Animals</subject><subject>Basic-Leucine Zipper Transcription Factors - genetics</subject><subject>Basic-Leucine Zipper Transcription Factors - metabolism</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - diagnosis</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain tumors</subject><subject>BTB and CNC homology 1 (BACH1)</subject><subject>Cell Line, Tumor</subject><subject>Cell self-renewal</subject><subject>Cerebrospinal fluid</subject><subject>Chemokines</subject><subject>Chemokines - metabolism</subject><subject>Colony-stimulating factor</subject><subject>Datasets as Topic</subject><subject>Decision making</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glioblastoma</subject><subject>Glioblastoma (GBM)</subject><subject>Glioblastoma - diagnosis</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - metabolism</subject><subject>Glioma cells</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Homology</subject><subject>Humans</subject><subject>Immune checkpoint</subject><subject>Immune response</subject><subject>Immunotherapy</subject><subject>Immunotherapy - methods</subject><subject>Macrophage Activation</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>Metastases</subject><subject>Molecular Targeted Therapy</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Nomograms</subject><subject>Prognosis</subject><subject>Risk</subject><subject>Scoring models</subject><subject>Stem cells</subject><subject>Survival Analysis</subject><subject>Therapeutic targets</subject><subject>Transcriptome sequencing</subject><subject>Transcriptomes</subject><subject>Tumor microenvironment</subject><subject>Tumor microenvironment (TME)</subject><subject>Tumor-Associated Macrophages - physiology</subject><subject>Tumors</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFLwzAYhoMoOqf_QKTgxUtnvqRtmoswhzph4EXPIc3SmdE2NUmF_XszOj148JTw8bxvvjwIXQGeAYbibjszXTBtPyOYQByVWQ5HaAIlK1NgOD-O97xgac4KfobOvd9iHOcZnKIzmnFCM0In6P5hvlhCIn0ik94GHStlkwTpNjoktXWJaduhs-FDO9nvEtMlm8bYqpE-2Fb6C3RSy8bry8M5Re9Pj2-LZbp6fX5ZzFepohyHlAAviCQV5cArYEopwmteYpbl67KuMMESKGEVY1jTkkNOCwpxVRl_IzGUdIpux97e2c9B-yBa45VuGtlpO3hBCiA4IzzmpujmD7q1g-vidpGiJeEYkz2VjZRy1nuna9E700q3E4DF3q_YitGv2PsVo98Yuz6UD1Wr17-hH6ERuB8BHW18Ge2EV0Z3Sq-N0yqItTX_v_AN0YqJ5Q</recordid><startdate>202202</startdate><enddate>202202</enddate><creator>Yuan, Feng</creator><creator>Cong, Zixiang</creator><creator>Cai, Xiangming</creator><creator>Zhu, Junhao</creator><creator>Yuan, Lei</creator><creator>Wang, Yingshuai</creator><creator>Tang, Chao</creator><creator>Ma, Chiyuan</creator><general>Elsevier B.V</general><general>Elsevier BV</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8132-9224</orcidid><orcidid>https://orcid.org/0000-0002-1710-5955</orcidid></search><sort><creationdate>202202</creationdate><title>BACH1 as a potential target for immunotherapy in glioblastomas</title><author>Yuan, Feng ; Cong, Zixiang ; Cai, Xiangming ; Zhu, Junhao ; Yuan, Lei ; Wang, Yingshuai ; Tang, Chao ; Ma, Chiyuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-21962a2b3919b17ccc29f980745d8fb020a1327b770e389153631041a187a0183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Basic-Leucine Zipper Transcription Factors - genetics</topic><topic>Basic-Leucine Zipper Transcription Factors - metabolism</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Brain cancer</topic><topic>Brain Neoplasms - diagnosis</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - metabolism</topic><topic>Brain tumors</topic><topic>BTB and CNC homology 1 (BACH1)</topic><topic>Cell Line, Tumor</topic><topic>Cell self-renewal</topic><topic>Cerebrospinal fluid</topic><topic>Chemokines</topic><topic>Chemokines - metabolism</topic><topic>Colony-stimulating factor</topic><topic>Datasets as Topic</topic><topic>Decision making</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glioblastoma</topic><topic>Glioblastoma (GBM)</topic><topic>Glioblastoma - diagnosis</topic><topic>Glioblastoma - genetics</topic><topic>Glioblastoma - metabolism</topic><topic>Glioma cells</topic><topic>Granulocyte-macrophage colony-stimulating factor</topic><topic>Homology</topic><topic>Humans</topic><topic>Immune checkpoint</topic><topic>Immune response</topic><topic>Immunotherapy</topic><topic>Immunotherapy - methods</topic><topic>Macrophage Activation</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>Metastases</topic><topic>Molecular Targeted Therapy</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Nomograms</topic><topic>Prognosis</topic><topic>Risk</topic><topic>Scoring models</topic><topic>Stem cells</topic><topic>Survival Analysis</topic><topic>Therapeutic targets</topic><topic>Transcriptome sequencing</topic><topic>Transcriptomes</topic><topic>Tumor microenvironment</topic><topic>Tumor microenvironment (TME)</topic><topic>Tumor-Associated Macrophages - physiology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Feng</creatorcontrib><creatorcontrib>Cong, Zixiang</creatorcontrib><creatorcontrib>Cai, Xiangming</creatorcontrib><creatorcontrib>Zhu, Junhao</creatorcontrib><creatorcontrib>Yuan, Lei</creatorcontrib><creatorcontrib>Wang, Yingshuai</creatorcontrib><creatorcontrib>Tang, Chao</creatorcontrib><creatorcontrib>Ma, Chiyuan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Feng</au><au>Cong, Zixiang</au><au>Cai, Xiangming</au><au>Zhu, Junhao</au><au>Yuan, Lei</au><au>Wang, Yingshuai</au><au>Tang, Chao</au><au>Ma, Chiyuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BACH1 as a potential target for immunotherapy in glioblastomas</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2022-02</date><risdate>2022</risdate><volume>103</volume><spage>108451</spage><epage>108451</epage><pages>108451-108451</pages><artnum>108451</artnum><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>•We confirmed that BACH1 as an independent prognostic indicator was enriched in glioblastomas.•BACH1 was strongly related to immune responses in glioblastoma, especially M0 and M2 tumour-associated macrophages mediated immune response.•We constructed polygenic risk scoring model and compound nomogram model based on BACH1, which might provide a reliable prognosis assessment tool.
Glioblastoma (GBM, WHO grade 4) is a highly heterogeneous and aggressive primary malignant brain tumor. BTB domain and CNC homology 1 (BACH1) is a transcription factor, and it plays an essential role in regulating tumor metastasis, tumor metabolism, and tumor stem cell self-renewal. However, its role in glioma is still unclear. In this research, we confirmed that BACH1 as an independent prognostic indicator was enriched in GBMs. BACH1 was strongly correlated with immune responses in GBMs, especially the M0 and M2 tumor-associated macrophage (TAM) mediated immune responses. GBMs with high expression of BACH1 express high levels of immune checkpoints (ICs), glioma cell-derived TAM chemokines, and M2 TAM markers. Interestingly, single cell RNA-seq analysis showed that the expression level of BACH1 in TAMs was higher than that in the other cell types in GBM. Transcriptome analysis of U87-MG cells showed that compared with the BACH1-vector U87-MG group, glioma cell-derived TAM chemokines (including monocyte chemotactic protein-1 (MCP-1), granulocyte–macrophage colony-stimulating factor (GM-CSF), and EGF) and ICs (including CD276, TIM-3, LAG3, TIGIT and LGALS9) were enriched in the BACH1-overexpressing U87-MG group. In addition, we constructed a polygenic risk scoring model and compound nomogram model based on BACH1, which might provide a reliable prognosis assessment tool for clinicians and aid in treatment decision-making in the clinic. In conclusion, this research identified that BACH1 might be a potential molecular signature for survival and immunotherapy response. GBMs with high expression of BACH1 have a stronger immunosuppressive tumor microenvironment (TME). Overexpression of BACH1 can upregulate the expression of glioma cell-derived TAM chemokines and ICs in vitro. Moreover, the risk model and nomogram model based on BACH1 can provide a reliable prognosis assessment tool. Therefore, BACH1 is a promising therapeutic target for GBMs.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>34923423</pmid><doi>10.1016/j.intimp.2021.108451</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-8132-9224</orcidid><orcidid>https://orcid.org/0000-0002-1710-5955</orcidid></addata></record> |
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| subjects | Animals Basic-Leucine Zipper Transcription Factors - genetics Basic-Leucine Zipper Transcription Factors - metabolism Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Brain cancer Brain Neoplasms - diagnosis Brain Neoplasms - genetics Brain Neoplasms - metabolism Brain tumors BTB and CNC homology 1 (BACH1) Cell Line, Tumor Cell self-renewal Cerebrospinal fluid Chemokines Chemokines - metabolism Colony-stimulating factor Datasets as Topic Decision making Gene expression Gene Expression Regulation, Neoplastic Glioblastoma Glioblastoma (GBM) Glioblastoma - diagnosis Glioblastoma - genetics Glioblastoma - metabolism Glioma cells Granulocyte-macrophage colony-stimulating factor Homology Humans Immune checkpoint Immune response Immunotherapy Immunotherapy - methods Macrophage Activation Medical prognosis Metabolism Metastases Molecular Targeted Therapy Monocyte chemoattractant protein 1 Monocytes Nomograms Prognosis Risk Scoring models Stem cells Survival Analysis Therapeutic targets Transcriptome sequencing Transcriptomes Tumor microenvironment Tumor microenvironment (TME) Tumor-Associated Macrophages - physiology Tumors |
| title | BACH1 as a potential target for immunotherapy in glioblastomas |
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