Work

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

Year: 2024

Type: article

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. • PLOD1 is highly expressed in THCA, PLOD1 can be used as a potential therapeutic target. • PLOD1 depletion inhibit THCA cell growth and metastasis by glycolysis • MAZ is identified as an upstream transcription factor of PLOD1 • Wnt/β-catenin pathway is activated by PLOD1 in THCA • PLOD1 depletion inhibit glycolysis by Wnt/β-catenin pathway

Source: Genomics

DOI: 10.1016/j.ygeno.2024.110943

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

Institutions: Shandong University, Second Hospital of Shandong University

Language: English

Topic: Wnt/β-catenin signaling in development and cancer

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $2,690