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Artemisinin derivatives maintain fibroblast normalization by acting on tumor-stroma interactions in oral tongue
Weixing Zeng1,2,3, Yawen Yang1,2,3, Jia Xiong1,4
1Kunming Medical University Kunming 650106, Yunnan, China.
Abstract:
Fibroblasts can transform into cancer-associated fibroblasts (CAFs) when continuously stimulated by cancer cells, thereby playing a crucial role in cancer progression. Growing evidence indicates that targeted therapy for CAF can influence tumor progression. Dihydroartemisinin (DHA) and artemether (ARM), semisynthetic derivatives of the natural compound artemisinin, have exhibited anticancer effects in various tumors. In this study, we found that tumor cells secreted platelet-derived growth factor-BB (PDGF-BB), which stimulated fibroblasts to transition into the CAF phenotype (cell phenotype and secretory phenotype). CAFs promote Cal-27 cell proliferation by secreting lactate. We focused on the mechanisms by which DHA and ARM affect the tumor-stroma interactions. These findings demonstrated that DHA and ARM effectively suppressed the secretion of PDGF-BB from Cal-27 cells, maintaining the normal state of hOMF and preventing the proliferative effect on Cal-27 cells. These findings were confirmed in xenograft models. Our study showed that artemisinin derivatives prevent the progression of oral tongue squamous cell carcinoma (OTSCC) by inhibiting the production of PDGF-BB in cancer cells to maintain the normal state of fibroblasts, thus providing a potential avenue for targeted OTSCC treatment.
Insights
Artemisinin derivatives like DHA and ARM inhibit oral tongue squamous cell carcinoma (OTSCC) progression. They work by blocking cancer cells from producing PDGF-BB, which prevents normal fibroblasts from becoming cancer-associated fibroblasts (CAFs).
Area of Science:
- Oncology
- Cancer Biology
- Pharmacology
Background:
- Cancer-associated fibroblasts (CAFs) promote tumor progression.
- Targeting CAFs is a promising therapeutic strategy.
- Artemisinin derivatives like dihydroartemisinin (DHA) and artemether (ARM) show anticancer potential.
Purpose of the Study:
- To investigate the mechanism of DHA and ARM in oral tongue squamous cell carcinoma (OTSCC).
- To explore how these artemisinin derivatives affect tumor-stroma interactions.
- To determine if DHA and ARM can prevent the transition of fibroblasts to CAFs.
Main Methods:
- Investigated the role of platelet-derived growth factor-BB (PDGF-BB) in fibroblast activation.
- Assessed the effect of DHA and ARM on PDGF-BB secretion by cancer cells.
- Evaluated the impact of DHA and ARM on fibroblast phenotype and function.
- Confirmed findings in xenograft models of OTSCC.
Main Results:
- Tumor cells secrete PDGF-BB, inducing fibroblasts to become CAFs.
- CAFs promote cancer cell proliferation via lactate secretion.
- DHA and ARM suppressed PDGF-BB secretion from cancer cells.
- DHA and ARM maintained normal fibroblast phenotype and inhibited cancer cell proliferation.
Conclusions:
- Artemisinin derivatives (DHA, ARM) inhibit OTSCC progression.
- These drugs prevent cancer cell-induced fibroblast activation by targeting PDGF-BB.
- This mechanism offers a potential therapeutic strategy for OTSCC.
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