Mediator complex subunit 1 promotes oral squamous cell carcinoma progression by activating MMP9 transcription and suppressing CD8


Journal

Journal of experimental & clinical cancer research : CR
ISSN: 1756-9966
Titre abrégé: J Exp Clin Cancer Res
Pays: England
ID NLM: 8308647

Informations de publication

Date de publication:
30 Sep 2024
Historique:
received: 06 06 2024
accepted: 13 09 2024
medline: 30 9 2024
pubmed: 30 9 2024
entrez: 29 9 2024
Statut: epublish

Résumé

The role of Mediator complex subunit 1 (MED1), a pivotal transcriptional coactivator implicated in diverse biological pathways, remains unexplored in the context of oral squamous cell carcinoma (OSCC). This study aims to elucidate the contributory mechanisms and potential impact of MED1 on the progression of OSCC. The expression and clinical significance of MED1 in OSCC tissues were evaluated through the bioinformatics analyses. The effects of MED1 on the biological behavior of OSCC cancer cells were assessed both in vitro and in vivo. Dual-luciferase reporter assay, chromatin immunoprecipitation (ChIP) assay, bioinformatic analysis, CD8 MED1 exhibited upregulation in both OSCC tissues and multiple OSCC cell lines, which correlated with decreased overall survival in patients. In vitro experiments demonstrated that knockdown of MED1 in metastatic OSCC cell lines SCC-9 and UPCI-SCC-154 hindered cell migration and invasion, while overexpression of MED1 promoted these processes. Whereas, MED1 knockdown had no impact on proliferation of cell lines mentioned above. In vivo studies further revealed that downregulation of MED1 effectively suppressed distant metastasis in OSCC. Mechanistically, MED1 enhanced the binding of transcription factors c-Jun and c-Fos to the matrix metalloprotein 9 (MMP9) promoters, resulting in a significant upregulation of MMP9 transcription. This process contributes to the migration and invasion of SCC-9 and UPCI-SCC-154 cells. Furthermore, MED1 modulated the expression of programmed death-ligand 1 (PD-L1) through the Notch signaling pathway, consequently impacting the tumor-killing capacity of CD8 Our findings indicate that MED1 plays a pivotal role in OSCC progression through the activation of MMP9 transcription and suppression of CD8

Sections du résumé

BACKGROUND BACKGROUND
The role of Mediator complex subunit 1 (MED1), a pivotal transcriptional coactivator implicated in diverse biological pathways, remains unexplored in the context of oral squamous cell carcinoma (OSCC). This study aims to elucidate the contributory mechanisms and potential impact of MED1 on the progression of OSCC.
METHODS METHODS
The expression and clinical significance of MED1 in OSCC tissues were evaluated through the bioinformatics analyses. The effects of MED1 on the biological behavior of OSCC cancer cells were assessed both in vitro and in vivo. Dual-luciferase reporter assay, chromatin immunoprecipitation (ChIP) assay, bioinformatic analysis, CD8
RESULTS RESULTS
MED1 exhibited upregulation in both OSCC tissues and multiple OSCC cell lines, which correlated with decreased overall survival in patients. In vitro experiments demonstrated that knockdown of MED1 in metastatic OSCC cell lines SCC-9 and UPCI-SCC-154 hindered cell migration and invasion, while overexpression of MED1 promoted these processes. Whereas, MED1 knockdown had no impact on proliferation of cell lines mentioned above. In vivo studies further revealed that downregulation of MED1 effectively suppressed distant metastasis in OSCC. Mechanistically, MED1 enhanced the binding of transcription factors c-Jun and c-Fos to the matrix metalloprotein 9 (MMP9) promoters, resulting in a significant upregulation of MMP9 transcription. This process contributes to the migration and invasion of SCC-9 and UPCI-SCC-154 cells. Furthermore, MED1 modulated the expression of programmed death-ligand 1 (PD-L1) through the Notch signaling pathway, consequently impacting the tumor-killing capacity of CD8
CONCLUSIONS CONCLUSIONS
Our findings indicate that MED1 plays a pivotal role in OSCC progression through the activation of MMP9 transcription and suppression of CD8

Identifiants

pubmed: 39343952
doi: 10.1186/s13046-024-03191-9
pii: 10.1186/s13046-024-03191-9
doi:

Substances chimiques

Matrix Metalloproteinase 9 EC 3.4.24.35
MMP9 protein, human EC 3.4.24.35
Mediator Complex Subunit 1 0
MED1 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

270

Informations de copyright

© 2024. The Author(s).

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Auteurs

Zhe Li (Z)

Department of Prosthodontics, Tianjin Medical University School and Hospital of Stomatology, Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University Institute of Stomatology, 12 Qixiangtai Road, Tianjin, 300070, China.

Mengke Sun (M)

Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, 22 Qixiangtai Road, Tianjin, 300070, China.

Ruimeng Yang (R)

Department of Prosthodontics, Tianjin Medical University School and Hospital of Stomatology, Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University Institute of Stomatology, 12 Qixiangtai Road, Tianjin, 300070, China.

Zheng Wang (Z)

Department of Prosthodontics, Tianjin Medical University School and Hospital of Stomatology, Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University Institute of Stomatology, 12 Qixiangtai Road, Tianjin, 300070, China.

Qianyu Zhu (Q)

Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, 22 Qixiangtai Road, Tianjin, 300070, China.

Yue Zhang (Y)

Department of Prosthodontics, Tianjin Medical University School and Hospital of Stomatology, Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University Institute of Stomatology, 12 Qixiangtai Road, Tianjin, 300070, China.

Haosun Yang (H)

Department of Prosthodontics, Tianjin Medical University School and Hospital of Stomatology, Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University Institute of Stomatology, 12 Qixiangtai Road, Tianjin, 300070, China.

Zhaosong Meng (Z)

Department of Oral and Maxillofacial Surgery, Tianjin Medical University School and Hospital of Stomatology, Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University Institue of Stomatology, 12 Qixiangtai Road, Tianjin, 300070, China. ddsmzs@sina.com.

Lizhi Hu (L)

Immunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, 22 Qixiangtai Road, Tianjin, 300070, China. lizhihu@tmu.edu.cn.

Lei Sui (L)

Department of Prosthodontics, Tianjin Medical University School and Hospital of Stomatology, Tianjin Key Laboratory of Oral Soft and Hard Tissues Restoration and Regeneration, Tianjin Medical University Institute of Stomatology, 12 Qixiangtai Road, Tianjin, 300070, China. suilei@tmu.edu.cn.

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