PLOD1 promote proliferation and migration with glycolysis via the Wnt/β-catenin pathway in THCA

IF 4.3 3区材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC

ACS Applied Electronic Materials Pub Date : 2024-10-16 DOI:10.1016/j.ygeno.2024.110943

Wei Cong, Jingfu Sun, Zhanyu Hao, Maosong Gong, Jianing Liu

{"title":"PLOD1 promote proliferation and migration with glycolysis via the Wnt/β-catenin pathway in THCA","authors":"Wei Cong, Jingfu Sun, Zhanyu Hao, Maosong Gong, Jianing Liu","doi":"10.1016/j.ygeno.2024.110943","DOIUrl":null,"url":null,"abstract":"<div><div>THCA (Thyroid carcinoma) is the most common endocrine malignancy in the world. The PLOD1 is highly expressed in THCA, but the mechanism is still unclear. It is found that the cell proliferation and migration were inhibited in si-PLOD1 group, and promoted with PLOD1 overexpression. MAZ is the transcription factor of PLOD1. The cell activities induced MAZ were reversed by si-PLOD1. The Glucose uptake, lactate production and ATP/ADP ratio were decreased with si-PLOD1. The glycolysis related proteins GLUT1, HK2, PFKP, PKM2, LDHA and Wnt/β-catenin pathway proteins WNT5A, cyclin D1, β-catenin were inhibited, GSK-3β is increased in si-PLOD1 group. BML-284 could reversed the si-PLOD1 effects on cell activities and Wnt/β-catenin pathway. The tumor xenografts were inhibited in si-PLOD1 group. As a potential therapeutic target, PLOD1 is regulated by MAZ in THCA. PLOD1 depletion could inhibit THCA cell proliferation and metastasis by glycolysis, which is inhibited by Wnt/β-catenin pathway in THCA.</div></div>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Electronic Materials","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0888754324001642","RegionNum":3,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENGINEERING, ELECTRICAL & ELECTRONIC","Score":null,"Total":0}

引用次数: 0

Abstract

THCA (Thyroid carcinoma) is the most common endocrine malignancy in the world. The PLOD1 is highly expressed in THCA, but the mechanism is still unclear. It is found that the cell proliferation and migration were inhibited in si-PLOD1 group, and promoted with PLOD1 overexpression. MAZ is the transcription factor of PLOD1. The cell activities induced MAZ were reversed by si-PLOD1. The Glucose uptake, lactate production and ATP/ADP ratio were decreased with si-PLOD1. The glycolysis related proteins GLUT1, HK2, PFKP, PKM2, LDHA and Wnt/β-catenin pathway proteins WNT5A, cyclin D1, β-catenin were inhibited, GSK-3β is increased in si-PLOD1 group. BML-284 could reversed the si-PLOD1 effects on cell activities and Wnt/β-catenin pathway. The tumor xenografts were inhibited in si-PLOD1 group. As a potential therapeutic target, PLOD1 is regulated by MAZ in THCA. PLOD1 depletion could inhibit THCA cell proliferation and metastasis by glycolysis, which is inhibited by Wnt/β-catenin pathway in THCA.

查看原文本刊更多论文

PLOD1通过Wnt/β-catenin途径促进THCA中糖酵解的增殖和迁移。

甲状腺癌（THCA）是世界上最常见的内分泌恶性肿瘤。PLOD1 在 THCA 中高表达，但其机制尚不清楚。研究发现，si-PLOD1 组细胞增殖和迁移受抑制，而 PLOD1 过表达组细胞增殖和迁移受促进。MAZ 是 PLOD1 的转录因子。si-PLOD1 逆转了 MAZ 诱导的细胞活性。si-PLOD1 可降低葡萄糖摄取、乳酸生成和 ATP/ADP 比率。糖酵解相关蛋白 GLUT1、HK2、PFKP、PKM2、LDHA 和 Wnt/β-catenin 通路蛋白 WNT5A、细胞周期蛋白 D1、β-catenin 在 si-PLOD1 组受到抑制，GSK-3β 在 si-PLOD1 组增加。BML-284 可逆转 si-PLOD1 对细胞活性和 Wnt/β-catenin 通路的影响。si-PLOD1组的肿瘤异种移植受到抑制。作为一个潜在的治疗靶点，PLOD1在THCA中受MAZ调控。抑制PLOD1可以通过糖酵解抑制THCA细胞的增殖和转移，而糖酵解在THCA中受到Wnt/β-catenin通路的抑制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

ACS Applied Electronic Materials Multiple-

CiteScore

7.20

自引率

4.30%

发文量

567