STAT-3, ELK-1, and c- Jun contributes IL-6 mediated ADAMTS-8 upregulation in colorectal cancer.

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Tác giả: Meltem Alper, Kübra Paspal Eroğlu, Yasemin Keleş, Saliha Derya Keskin, Feray Köçkar, Feyza Nur Sav

Ngôn ngữ: eng

Ký hiệu phân loại: 202.117 Relation to the world

Thông tin xuất bản: Netherlands : Molecular biology reports , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 214468

BACKGROUND: ADAMTSs are extracellular matrix metalloproteinases that mainly process extracellular matrix components and closely related tumorigenesis. ADAMTS-8 is an anti-angiogenic member of the family and is dysregulated in common cancers. The tumor suppressor function of the ADAMTS-8 has been demonstrated in colorectal cancer. Although ADAMTS-8 plays a critical role in tumor progression, transcriptional regulatory features haven't been studied yet. MATERIALS AND METHODS: The human ADAMTS-8 promoter was cloned into the pMetLuc Reporter vector. Basal promoter activity and the effect of the IL-6 on ADAMTS-8 promoter activity were determined by transient transfection assays in SW480 cells. QRT-PCR and Western blot analyses assessed the impact of IL-6 on ADAMTS-8 mRNA and protein expressions. Functional binding of the specific transcription factors to the ADAMTS-8 promoter region was evaluated by ChIP qPCR and EMSA. RESULTS: Our results demonstrated that the ADAMTS-8 promoter includes multiple binding sites for transcription factors that could be activated in the inflammatory pathways. IL-6 stimulation increased ADAMTS-8 promoter activity, also mRNA, and protein expressions. Pathway inhibition studies showed that IL-6-mediated induction of ADAMTS-8 was achieved through p38/MAPK, NF-κB, PI3K, and SAPK/JNK pathways. STATs, Elk-1, and c-Jun functionally bind to the ADAMTS-8 promoter region. CONCLUSION: It can be concluded that inflammation is a strong positive regulator of the ADAMTS-8 gene.
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