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

Wei Cong1, Jingfu Sun1, Zhanyu Hao1

  • 1Department of Thyroid Surgery, The Second Hospital of Shandong University, Shandong University, Shandong Province, PR China.

Genomics
|October 18, 2024
PubMed

Insights

Thyroid carcinoma (THCA) cell growth and metastasis are inhibited by targeting PLOD1. This mechanism involves the regulation of glycolysis and the Wnt/β-catenin pathway, suggesting PLOD1 as a potential therapeutic target.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Thyroid carcinoma (THCA) is a prevalent endocrine malignancy.
  • Lysyl hydroxylase 1 (PLOD1) is overexpressed in THCA, but its functional role remains unclear.
  • MAZ acts as a transcription factor for PLOD1.

Purpose of the Study:

  • To investigate the role of PLOD1 in THCA progression.
  • To elucidate the regulatory mechanisms of PLOD1 in THCA.
  • To explore PLOD1 as a potential therapeutic target for THCA.

Main Methods:

  • Utilized si-PLOD1 to deplete PLOD1 expression and PLOD1 overexpression in THCA cells.
  • Assessed cell proliferation, migration, glucose uptake, lactate production, and ATP/ADP ratio.
  • Analyzed key glycolysis and Wnt/β-catenin pathway proteins.
  • Investigated the effect of BML-284, a Wnt/β-catenin inhibitor.
  • Evaluated tumor xenograft growth in vivo.

Main Results:

  • PLOD1 depletion inhibited THCA cell proliferation and migration, while PLOD1 overexpression promoted these activities.
  • Glucose metabolism, including uptake, lactate production, and ATP/ADP ratio, was reduced upon PLOD1 depletion.
  • Expression of glycolysis proteins (GLUT1, HK2, PFKP, PKM2, LDHA) and Wnt/β-catenin pathway proteins (WNT5A, cyclin D1, β-catenin) was downregulated, with increased GSK-3β.
  • BML-284 reversed the effects of si-PLOD1 on cell activities and the Wnt/β-catenin pathway.
  • Tumor xenograft growth was significantly inhibited in the si-PLOD1 group.

Conclusions:

  • PLOD1, regulated by MAZ, plays a crucial role in THCA progression.
  • PLOD1 depletion inhibits THCA cell proliferation and metastasis by suppressing glycolysis via the Wnt/β-catenin pathway.
  • PLOD1 represents a promising therapeutic target for thyroid carcinoma.
Keywords:
GlycolysisMAZPLOD1ProliferationThyroid carcinomaWnt/β-catenin pathway

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