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Published in: Cancer Cell International 1/2024

Open Access 01-12-2024 | Research

PDGF-BB accelerates TSCC via fibroblast lactates limiting miR-26a-5p and boosting mitophagy

Authors: Jianguo Xu, Li Bian, Dingyun You, Ziliang Li, Tingting Wang, Yiting Li, Xiaobin Ren, Yongwen He

Published in: Cancer Cell International | Issue 1/2024

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Abstract

The tumor microenvironment and cancer-associated fibroblasts (CAFs) play crucial roles in tumor development, and their metabolic coupling remains unclear. Clinical data showed a positive correlation between PDGF-BB, CAFs, and glycolysis in the tumor microenvironment of oral tongue squamous cell carcinoma patients. In vitro, CAFs are derived from hOMF cells treated with PDGF-BB, which induces their formation and promotes aerobic glycolysis. Mitophagy increased the PDGF-BB-induced formation of CAF phenotypes and aerobic glycolysis, while autophagy inhibition blocked PDGF-BB-induced effects. Downregulation of miR-26a-5p was observed in CAFs; upregulation of miR-26a-5p inhibited the expression of mitophagy-related proteins ULKI, Parkin, PINK1, and LC3 and aerobic glycolysis in PDGF-BB-induced CAFs. PDGF-BB-induced CAFs promoted tumor cell proliferation, invasion, metastasis, NF-κB signaling pathway activation, and PDGF-BB secretion. Thus, PDGF-BB is associated with lactate-induced CAF formation and glucose metabolism reprogramming. These findings indicate potential therapeutic targets in oral tongue squamous cell carcinoma.
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Metadata
Title
PDGF-BB accelerates TSCC via fibroblast lactates limiting miR-26a-5p and boosting mitophagy
Authors
Jianguo Xu
Li Bian
Dingyun You
Ziliang Li
Tingting Wang
Yiting Li
Xiaobin Ren
Yongwen He
Publication date
01-12-2024
Publisher
BioMed Central
Published in
Cancer Cell International / Issue 1/2024
Electronic ISSN: 1475-2867
DOI
https://doi.org/10.1186/s12935-023-03172-6

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