4.7 Article

Resveratrol inhibits proliferation, migration and invasion of multiple myeloma cells via NEAT1-mediated Wnt/beta-catenin signaling pathway

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 107, Issue -, Pages 484-494

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2018.08.003

Keywords

Multiple myeloma; Resveratrol; NEAT1; Wnt/beta-catenin signaling pathway; Unfolded; Protein response

Funding

  1. Technology Development Program of Jilin Province [20150204082SF]

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Purpose: To study the influence of resveratrol on proliferation, migration and invasion of multiple myeloma (MM) cells through the long noncoding RNA (lncRNA) NEAT1 (nuclear enriched abundant transcript 1)-modulated Wnt/beta-catenin signaling pathway. Methods: Microarray analysis was used to screen aberrantly expressed lncRNAs from MM cells and normal plasmocytes. The effects of NEAT1 overexpression/silencing or resveratrol treatment on MM cell (U266 and LP1) proliferation, migration and invasion were investigated using CCK-8 (Cell Counting Kit-8), wound healing and Transwell invasion assays. Expression of Wnt/beta-catenin related proteins and unfolded protein response (UPR)-related proteins was detected by western blot. Results: lncRNA NEAT1 was highly expressed in MM cells, which could be significantly inhibited by resveratrol. NEAT1 overexpression induced proliferation, migration and invasion of MM cells, while resveratrol counteracted its effect. NEAT1 upregulated protein expression in the Wnt/beta-catenin signaling pathway, while resveratrol reversed the negative effect of NEAT1 overexpression on MM cells through the Wnt/beta-catenin signaling pathway, and hence suppressed MM cell reproduction, migration and invasion. Resveratrol could also restrain unfolded protein response in MM cells. Conclusion: Resveratrol downregulated the expression of lncRNA NEAT1 in MM cells and inhibited proliferation, migration and invasion of MM cells by suppressing the Wnt/beta-catenin signaling pathway and unfolded protein response.

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