Hypoxia-induced PLOD1 overexpression contributes to the malignant phenotype of glioblastoma via NF-κB signaling
Procollagen lysyl hydroxylase 1 (PLOD1) is highly expressed in malignant tumors such as esophageal squamous cell carcinoma, gastric cancer, and colorectal cancer. Bioinformatics analysis revealed that PLOD1 is associated with the progression of GBM, particularly the most malignant mesenchymal subtyp...
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| Veröffentlicht in: | Oncogene 2021-02, Vol.40 (8), p.1458-1475 |
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| description | Procollagen lysyl hydroxylase 1 (PLOD1) is highly expressed in malignant tumors such as esophageal squamous cell carcinoma, gastric cancer, and colorectal cancer. Bioinformatics analysis revealed that PLOD1 is associated with the progression of GBM, particularly the most malignant mesenchymal subtype (MES). Moreover, in the TCGA and CGGA datasets, the mean survival time of patients with high PLOD1 expression was significantly shorter than that of patients with low expression. The clinical samples confirmed this result. Therefore, we aimed to investigate the effect of PLOD1 on the development of mesenchymal GBM in vitro and in vivo and its possible mechanisms. Molecular experiments were conducted on the patient-derived glioma stem cells and found that PLOD1 expressed higher in tumor tissues and cancer cell lines of patients with GBM, especially in the MES. PLOD1 also enhanced tumor viability, proliferation, migration, and promoted MES transition while inhibited apoptosis. Tumor xenograft results also indicated that PLOD1 overexpression significantly promotes malignant behavior of tumors. Mechanistically, bioinformatics analysis further revealed that PLOD1 expression was closely associated with the NF-κB signaling pathway. Besides, we also found that hypoxic environments also enhanced the tumor-promoting effects of PLOD1. In conclusion, overexpression of PLOD1 may be an important factor in the enhanced invasiveness and MES transition of GBM. Thus, PLOD1 is a potential treatment target for mesenchymal GBM or even all GBM. |
| doi_str_mv | 10.1038/s41388-020-01635-y |
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Bioinformatics analysis revealed that PLOD1 is associated with the progression of GBM, particularly the most malignant mesenchymal subtype (MES). Moreover, in the TCGA and CGGA datasets, the mean survival time of patients with high PLOD1 expression was significantly shorter than that of patients with low expression. The clinical samples confirmed this result. Therefore, we aimed to investigate the effect of PLOD1 on the development of mesenchymal GBM in vitro and in vivo and its possible mechanisms. Molecular experiments were conducted on the patient-derived glioma stem cells and found that PLOD1 expressed higher in tumor tissues and cancer cell lines of patients with GBM, especially in the MES. PLOD1 also enhanced tumor viability, proliferation, migration, and promoted MES transition while inhibited apoptosis. Tumor xenograft results also indicated that PLOD1 overexpression significantly promotes malignant behavior of tumors. Mechanistically, bioinformatics analysis further revealed that PLOD1 expression was closely associated with the NF-κB signaling pathway. Besides, we also found that hypoxic environments also enhanced the tumor-promoting effects of PLOD1. In conclusion, overexpression of PLOD1 may be an important factor in the enhanced invasiveness and MES transition of GBM. Thus, PLOD1 is a potential treatment target for mesenchymal GBM or even all GBM.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-020-01635-y</identifier><identifier>PMID: 33420370</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/89 ; 42/100 ; 631/67/1922 ; 631/67/71 ; 64/60 ; Animals ; Apoptosis ; Apoptosis - genetics ; Bioinformatics ; Brain cancer ; Brain tumors ; Cancer ; Cell Biology ; Cell Line, Tumor ; Cell Proliferation - genetics ; Colorectal carcinoma ; Databases, Factual ; Esophagus ; Female ; Gastric cancer ; Gene Expression Regulation, Neoplastic - genetics ; Glioblastoma ; Glioblastoma - genetics ; Glioblastoma - pathology ; Glioma cells ; Human Genetics ; Humans ; Hydroxylase ; Hypoxia ; Internal Medicine ; Invasiveness ; Kaplan-Meier Estimate ; Male ; Medicine ; Medicine & Public Health ; Mesenchyme ; NF-kappa B - genetics ; NF-κB protein ; Oncology ; Patients ; Phenotype ; Phenotypes ; Procollagen ; Procollagen-lysine 5-dioxygenase ; Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase - genetics ; Signal transduction ; Signal Transduction - genetics ; Squamous cell carcinoma ; Stem cells ; Transcription Factor RelA - genetics ; Tumor cell lines ; Tumor Hypoxia - genetics ; Tumors ; Xenografts</subject><ispartof>Oncogene, 2021-02, Vol.40 (8), p.1458-1475</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-5601a37e843acef0e52d9aafcdbfe95b15583ec7221a5ff7c3375d6f099a75693</citedby><cites>FETCH-LOGICAL-c474t-5601a37e843acef0e52d9aafcdbfe95b15583ec7221a5ff7c3375d6f099a75693</cites><orcidid>0000-0001-8947-0604 ; 0000-0002-5790-1307</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41388-020-01635-y$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41388-020-01635-y$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33420370$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Zhenlin</creatorcontrib><creatorcontrib>Shi, Yuping</creatorcontrib><creatorcontrib>Ying, Chenting</creatorcontrib><creatorcontrib>Jiang, Yang</creatorcontrib><creatorcontrib>Hu, Jiangfeng</creatorcontrib><title>Hypoxia-induced PLOD1 overexpression contributes to the malignant phenotype of glioblastoma via NF-κB signaling</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Procollagen lysyl hydroxylase 1 (PLOD1) is highly expressed in malignant tumors such as esophageal squamous cell carcinoma, gastric cancer, and colorectal cancer. Bioinformatics analysis revealed that PLOD1 is associated with the progression of GBM, particularly the most malignant mesenchymal subtype (MES). Moreover, in the TCGA and CGGA datasets, the mean survival time of patients with high PLOD1 expression was significantly shorter than that of patients with low expression. The clinical samples confirmed this result. Therefore, we aimed to investigate the effect of PLOD1 on the development of mesenchymal GBM in vitro and in vivo and its possible mechanisms. Molecular experiments were conducted on the patient-derived glioma stem cells and found that PLOD1 expressed higher in tumor tissues and cancer cell lines of patients with GBM, especially in the MES. PLOD1 also enhanced tumor viability, proliferation, migration, and promoted MES transition while inhibited apoptosis. Tumor xenograft results also indicated that PLOD1 overexpression significantly promotes malignant behavior of tumors. Mechanistically, bioinformatics analysis further revealed that PLOD1 expression was closely associated with the NF-κB signaling pathway. Besides, we also found that hypoxic environments also enhanced the tumor-promoting effects of PLOD1. In conclusion, overexpression of PLOD1 may be an important factor in the enhanced invasiveness and MES transition of GBM. Thus, PLOD1 is a potential treatment target for mesenchymal GBM or even all GBM.</description><subject>13/89</subject><subject>42/100</subject><subject>631/67/1922</subject><subject>631/67/71</subject><subject>64/60</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Bioinformatics</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Colorectal carcinoma</subject><subject>Databases, Factual</subject><subject>Esophagus</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Glioblastoma</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - pathology</subject><subject>Glioma cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hydroxylase</subject><subject>Hypoxia</subject><subject>Internal Medicine</subject><subject>Invasiveness</subject><subject>Kaplan-Meier Estimate</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mesenchyme</subject><subject>NF-kappa B - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Zhenlin</au><au>Shi, Yuping</au><au>Ying, Chenting</au><au>Jiang, Yang</au><au>Hu, Jiangfeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypoxia-induced PLOD1 overexpression contributes to the malignant phenotype of glioblastoma via NF-κB signaling</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2021-02-25</date><risdate>2021</risdate><volume>40</volume><issue>8</issue><spage>1458</spage><epage>1475</epage><pages>1458-1475</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><abstract>Procollagen lysyl hydroxylase 1 (PLOD1) is highly expressed in malignant tumors such as esophageal squamous cell carcinoma, gastric cancer, and colorectal cancer. Bioinformatics analysis revealed that PLOD1 is associated with the progression of GBM, particularly the most malignant mesenchymal subtype (MES). Moreover, in the TCGA and CGGA datasets, the mean survival time of patients with high PLOD1 expression was significantly shorter than that of patients with low expression. The clinical samples confirmed this result. Therefore, we aimed to investigate the effect of PLOD1 on the development of mesenchymal GBM in vitro and in vivo and its possible mechanisms. Molecular experiments were conducted on the patient-derived glioma stem cells and found that PLOD1 expressed higher in tumor tissues and cancer cell lines of patients with GBM, especially in the MES. PLOD1 also enhanced tumor viability, proliferation, migration, and promoted MES transition while inhibited apoptosis. Tumor xenograft results also indicated that PLOD1 overexpression significantly promotes malignant behavior of tumors. Mechanistically, bioinformatics analysis further revealed that PLOD1 expression was closely associated with the NF-κB signaling pathway. Besides, we also found that hypoxic environments also enhanced the tumor-promoting effects of PLOD1. In conclusion, overexpression of PLOD1 may be an important factor in the enhanced invasiveness and MES transition of GBM. Thus, PLOD1 is a potential treatment target for mesenchymal GBM or even all GBM.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>33420370</pmid><doi>10.1038/s41388-020-01635-y</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0001-8947-0604</orcidid><orcidid>https://orcid.org/0000-0002-5790-1307</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/89 42/100 631/67/1922 631/67/71 64/60 Animals Apoptosis Apoptosis - genetics Bioinformatics Brain cancer Brain tumors Cancer Cell Biology Cell Line, Tumor Cell Proliferation - genetics Colorectal carcinoma Databases, Factual Esophagus Female Gastric cancer Gene Expression Regulation, Neoplastic - genetics Glioblastoma Glioblastoma - genetics Glioblastoma - pathology Glioma cells Human Genetics Humans Hydroxylase Hypoxia Internal Medicine Invasiveness Kaplan-Meier Estimate Male Medicine Medicine & Public Health Mesenchyme NF-kappa B - genetics NF-κB protein Oncology Patients Phenotype Phenotypes Procollagen Procollagen-lysine 5-dioxygenase Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase - genetics Signal transduction Signal Transduction - genetics Squamous cell carcinoma Stem cells Transcription Factor RelA - genetics Tumor cell lines Tumor Hypoxia - genetics Tumors Xenografts |
| title | Hypoxia-induced PLOD1 overexpression contributes to the malignant phenotype of glioblastoma via NF-κB signaling |
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