The Nexus of Inflammation-Induced Epithelial-Mesenchymal Transition and Lung Cancer Progression: A Roadmap to Pentacyclic Triterpenoid-Based Therapies

Lung cancer is the leading cause of cancer-related death worldwide. Its high mortality is partly due to chronic inflammation that accompanies the disease and stimulates cancer progression. In this review, we analyzed recent studies and highlighted the role of the epithelial-mesenchymal transition (E...

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Bibliographic Details
Published in:International journal of molecular sciences 2023-12, Vol.24 (24), p.17325
Main Authors: Odarenko, Kirill V, Zenkova, Marina A, Markov, Andrey V
Format: Article
Language:English
Subjects:
aggressiveness
Cell adhesion & migration
Chronic obstructive pulmonary disease
Collagen
COVID-19
Cytokines
Drug development
epithelial-to-mesenchymal transition
Fibroblasts
Genotype & phenotype
Growth factors
Inflammation
Lung cancer
Metastasis
natural products
pulmonary malignancy
Transcription factors
tumor stem cells
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Summary:Lung cancer is the leading cause of cancer-related death worldwide. Its high mortality is partly due to chronic inflammation that accompanies the disease and stimulates cancer progression. In this review, we analyzed recent studies and highlighted the role of the epithelial-mesenchymal transition (EMT) as a link between inflammation and lung cancer. In the inflammatory tumor microenvironment (iTME), fibroblasts, macrophages, granulocytes, and lymphocytes produce inflammatory mediators, some of which can induce EMT. This leads to increased invasiveness of tumor cells and self-renewal of cancer stem cells (CSCs), which are associated with metastasis and tumor recurrence, respectively. Based on published data, we propose that inflammation-induced EMT may be a potential therapeutic target for the treatment of lung cancer. This prospect is partially realized in the development of EMT inhibitors based on pentacyclic triterpenoids (PTs), described in the second part of our study. PTs reduce the metastatic potential and stemness of tumor cells, making PTs promising candidates for lung cancer therapy. We emphasize that the high diversity of molecular mechanisms underlying inflammation-induced EMT far exceeds those that have been implicated in drug development. Therefore, analysis of information on the relationship between the iTME and EMT is of great interest and may provide ideas for novel treatment approaches for lung cancer.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms242417325