Journal Article Review Ppublish 1 citation
PubMed: 39593276 DOI: 10.20892/j.issn.2095-3941.2024.0320
Modulation of gut microbiota in targeted cancer therapy: insights on the EGFR/VEGF/KRAS pathways.
Cancer Biol Med 21(12)
Authors: Li Gong, Shixue Yang, Junli Huang, Yongsheng Li
Affiliations
- Department of Phase I Clinical Trial Ward, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing 400030, China. Key Laboratory of Biorheological Science and Technology of Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, China.
- Department of Medical Oncology, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing 400030, China.
- Key Laboratory of Biorheological Science and Technology of Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, China.
- Department of Phase I Clinical Trial Ward, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing 400030, China.
Abstract
The rise in the incidence of cancer globally has led to a heightened interest in targeted therapies as a form of anticancer treatment. Key oncogenic targets, including epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and kirsten rat sarcoma viral oncogene homologue (KRAS), have emerged as focal points in the development of targeted agents. Research has investigated the impact of gut microbiota on the efficacy of various anticancer therapies, such as immunotherapy, chemotherapy, and radiotherapy. However, a notable gap exists in the literature regarding the relationship between gut microbiota and targeted agents. This review emphasizes how specific gut microbiota and gut microbiota metabolites, including butyrate, propionate, and ursodeoxycholic acid, interact with oncogenic pathways to modulate anti-tumor effects. Conversely, deoxycholic acid, lipopolysaccharide, and trimethylamine n-oxide may exert pro-tumor effects. Furthermore, modulation of the gut microbiota influences glucose and lipid metabolism, thereby enhancing the response to anti-KRAS agents and addressing diarrhea induced by tyrosine kinase inhibitors. By elucidating the connection between gut microbiota and the EGFR/VEGF/KRAS pathways, this review provides valuable insights for advancing targeted cancer therapy and optimizing treatment outcomes in clinical settings.
MeSH
Growth, Vascular Endothelial Growth Factor A, Deoxycholic Acid, Neoplasms, Therapeutics, Gastrointestinal Microbiome, Microbiota