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从（Oliv.）Diels中提取的多糖通过调节miR-373-3p介导的TGF-β/Smad4信号通路减轻胶质瘤细胞的恶性特征。

Polysaccharides Extracted from (Oliv.) Diels Relieve the Malignant Characteristics of Glioma Cells through Regulating the MiR-373-3p-Mediated TGF-/Smad4 Signaling Pathway.

作者信息

Qu Chunhong, Dong Weifeng

机构信息

Department of Critical Care Medicine, The First People's Hospital of Xiaoshan Hangzhou, Hangzhou 311200, China.

Department of Neurosurgery, The First People's Hospital of Xiaoshan Hangzhou, Hangzhou 311200, China.

出版信息

Evid Based Complement Alternat Med. 2022 Jul 9;2022:7469774. doi: 10.1155/2022/7469774. eCollection 2022.

DOI:10.1155/2022/7469774
PMID:35855826
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9288290/
Abstract

OBJECTIVES

polysaccharide (ASP) is a traditional herbal medicine accompanied by antitumor potential. This study aims to explore the therapeutic potential of ASP on glioma, as well as the underlying mechanisms involving microRNA-373-3p (miR-373-3p) and the TGF-/Smad4 signaling pathway.

METHODS

U251 cells (a human glioma cell line) were treated with different concentrations of ASP. miR-373-3p was silenced in U251 cells by the transfection of the miR-373-3p inhibitor. Cell viability and apoptosis were measured by CCK-8 assay and flow cytometry, respectively. Cell migration and invasion were detected by wound healing and transwell assays, respectively. The miR-373-3p expression was measured by RT-qPCR. The protein expressions of TGF- and Smad4 were evaluated by both western blotting and immunofluorescence.

RESULTS

ASP inhibited the viability, migration, and invasion, and enhanced the apoptosis of U251 cells in a dose-dependent manner. ASP increased miR-373-3p expression and decreased TGF- and Smad4 expressions in U251 cells. Silencing of miR-373-3p weakened the effects of ASP on inhibiting cell viability, migration, and invasion, as well as promoting cell apoptosis. In addition, deleting miR-373-3p weakened the inhibiting effects of ASP on the TGF-/Smad4 pathway in U251 cells.

CONCLUSIONS

ASP suppresses the malignant progression of glioma via regulating the miR-373-3p-mediated TGF-/Smad4 pathway.

摘要

目的

云芝多糖（ASP）是一种具有抗肿瘤潜力的传统草药。本研究旨在探讨ASP对胶质瘤的治疗潜力，以及涉及微小RNA - 373 - 3p（miR - 373 - 3p）和转化生长因子-β/ Smad4信号通路的潜在机制。

方法

用不同浓度的ASP处理U251细胞（一种人胶质瘤细胞系）。通过转染miR - 373 - 3p抑制剂使U251细胞中的miR - 373 - 3p沉默。分别通过CCK - 8法和流式细胞术检测细胞活力和凋亡。分别通过伤口愈合试验和Transwell试验检测细胞迁移和侵袭。通过RT - qPCR检测miR - 373 - 3p表达。通过蛋白质印迹法和免疫荧光法评估转化生长因子-β和Smad4的蛋白表达。

结果

ASP以剂量依赖性方式抑制U251细胞的活力、迁移和侵袭，并增强其凋亡。ASP增加U251细胞中miR - 373 - 3p表达，并降低转化生长因子-β和Smad4表达。miR - 373 - 3p沉默减弱了ASP对抑制细胞活力、迁移和侵袭以及促进细胞凋亡的作用。此外，缺失miR - 373 - 3p减弱了ASP对U251细胞中转化生长因子-β/ Smad4通路的抑制作用。

结论

ASP通过调节miR - 373 - 3p介导的转化生长因子-β/ Smad4通路抑制胶质瘤的恶性进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/3196b3be3345/ECAM2022-7469774.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/bfebb777c57e/ECAM2022-7469774.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/97ee6bbabc00/ECAM2022-7469774.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/b5d394608fc2/ECAM2022-7469774.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/3196b3be3345/ECAM2022-7469774.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/bfebb777c57e/ECAM2022-7469774.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/97ee6bbabc00/ECAM2022-7469774.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/b5d394608fc2/ECAM2022-7469774.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9509/9288290/3196b3be3345/ECAM2022-7469774.004.jpg

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