Cited 0 times in Scipus Cited Count

Transcriptional regulatory networks of tumor-associated macrophages that drive malignancy in mesenchymal glioblastoma

DC Field Value Language
dc.contributor.authorSa, JK-
dc.contributor.authorChang, N-
dc.contributor.authorLee, HW-
dc.contributor.authorCho, HJ-
dc.contributor.authorCeccarelli, M-
dc.contributor.authorCerulo, L-
dc.contributor.authorYin, J-
dc.contributor.authorKim, SS-
dc.contributor.authorCaruso, FP-
dc.contributor.authorLee, M-
dc.contributor.authorKim, D-
dc.contributor.authorOh, YT-
dc.contributor.authorLee, Y-
dc.contributor.authorHer, NG-
dc.contributor.authorMin, B-
dc.contributor.authorKim, HJ-
dc.contributor.authorJeong, DE-
dc.contributor.authorKim, HM-
dc.contributor.authorKim, H-
dc.contributor.authorChung, S-
dc.contributor.authorWoo, HG-
dc.contributor.authorLee, J-
dc.contributor.authorKong, DS-
dc.contributor.authorSeol, HJ-
dc.contributor.authorLee, JI-
dc.contributor.authorKim, J-
dc.contributor.authorPark, WY-
dc.contributor.authorWang, Q-
dc.contributor.authorSulman, EP-
dc.contributor.authorHeimberger, AB-
dc.contributor.authorLim, M-
dc.contributor.authorPark, JB-
dc.contributor.authorIavarone, A-
dc.contributor.authorVerhaak, RGW-
dc.contributor.authorNam, DH-
dc.date.accessioned2022-11-29T01:43:35Z-
dc.date.available2022-11-29T01:43:35Z-
dc.date.issued2020-
dc.identifier.issn1474-7596-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/23026-
dc.description.abstractBACKGROUND: Glioblastoma (GBM) is a complex disease with extensive molecular and transcriptional heterogeneity. GBM can be subcategorized into four distinct subtypes; tumors that shift towards the mesenchymal phenotype upon recurrence are generally associated with treatment resistance, unfavorable prognosis, and the infiltration of pro-tumorigenic macrophages. RESULTS: We explore the transcriptional regulatory networks of mesenchymal-associated tumor-associated macrophages (MA-TAMs), which drive the malignant phenotypic state of GBM, and identify macrophage receptor with collagenous structure (MARCO) as the most highly differentially expressed gene. MARCO(high) TAMs induce a phenotypic shift towards mesenchymal cellular state of glioma stem cells, promoting both invasive and proliferative activities, as well as therapeutic resistance to irradiation. MARCO(high) TAMs also significantly accelerate tumor engraftment and growth in vivo. Moreover, both MA-TAM master regulators and their target genes are significantly correlated with poor clinical outcomes and are often associated with genomic aberrations in neurofibromin 1 (NF1) and phosphoinositide 3-kinases/mammalian target of rapamycin/Akt pathway (PI3K-mTOR-AKT)-related genes. We further demonstrate the origination of MA-TAMs from peripheral blood, as well as their potential association with tumor-induced polarization states and immunosuppressive environments. CONCLUSIONS: Collectively, our study characterizes the global transcriptional profile of TAMs driving mesenchymal GBM pathogenesis, providing potential therapeutic targets for improving the effectiveness of GBM immunotherapy.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHCarcinogenesis-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHGene Expression Regulation, Neoplastic-
dc.subject.MESHGene Regulatory Networks-
dc.subject.MESHGlioblastoma-
dc.subject.MESHGlioma-
dc.subject.MESHHumans-
dc.subject.MESHImmunotherapy-
dc.subject.MESHMacrophages-
dc.subject.MESHMice-
dc.subject.MESHNeurofibromin 1-
dc.subject.MESHPhenotype-
dc.subject.MESHPrognosis-
dc.subject.MESHStem Cells-
dc.subject.MESHTranscriptome-
dc.subject.MESHTumor Microenvironment-
dc.subject.MESHTumor-Associated Macrophages-
dc.titleTranscriptional regulatory networks of tumor-associated macrophages that drive malignancy in mesenchymal glioblastoma-
dc.typeArticle-
dc.identifier.pmid32847614-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7448990-
dc.contributor.affiliatedAuthorWoo, HG-
dc.type.localJournal Papers-
dc.identifier.doi10.1186/s13059-020-02140-x-
dc.citation.titleGenome biology-
dc.citation.volume21-
dc.citation.number1-
dc.citation.date2020-
dc.citation.startPage216-
dc.citation.endPage216-
dc.identifier.bibliographicCitationGenome biology, 21(1). : 216-216, 2020-
dc.identifier.eissn1474-760X-
dc.relation.journalidJ014747596-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
Files in This Item:
32847614.pdfDownload

qrcode

해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse