Journal
PHARMACOLOGICAL RESEARCH
Volume 186, Issue -, Pages -Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2022.106534
Keywords
Colorectal cancer; Micro RNA; Cancer-associated fibroblast; Exosomal; Epithelial-mesenchymal transformation; Chemotherapeutic resistance
Categories
Funding
- Medical and Health Science and Technology Development Project of Shandong Province [202002060904]
- 2021 High-level Research Cultivation Project of Jining Medical University [JYGC2021KJ011]
- Innovation Team of Integrated Chinese and Western Medicine Treatment of Spleen and Stomach Diseases, Jining Medical University [18]
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The current study aimed to assess the role and potential mechanism of miR-625-3p released by cancer-associated fibroblasts (CAFs) in colorectal cancer (CRC) cells. The results indicated that miR-625-3p released by CAFs might promote the migration, invasion, epithelial-mesenchymal transformation (EMT), and chemotherapeutic resistance in CRC cells by inhibiting the CELF2/WWOX pathway.
Migration, invasion, epithelial-mesenchymal transformation (EMT), and chemotherapeutic resistance are the leading causes of therapeutic failure in people with colorectal cancer (CRC). The migration of exosomal miRNA between cancer cells and the tumor microenvironment is directly associated with malignant behavior in cancer -associated fibroblasts (CAFs). In the context of earlier research, the purpose of the current study was to assess the role and potential mechanism of miR-625-3p released by CAFs in CRC cells. Exosomes were extracted and pu-rified from CAFs conditioned medium by ultracentrifugation. Western blot, immunohistochemistry, CCK-8, transwell assay, H&E staining, Tunnel, real-time PCR, double luciferase assay, RNA-binding protein immuno-precipitation (RIP), and immunofluorescence double staining experiments were used to investigate the effects of CAFs-Exo and miR-625-3p on CRC cell invasion, migration, proliferation, EMT, chemotherapeutic resistance, and molecular mechanisms. The current results indicated that CAFs-Exo was directly internalized by CRC cells, and exosomal miR-625-3p derived from CAFs might promote migration, invasion, EMT and chemotherapeutic resistance in CRC cells by inhibiting the CELF2/WWOX pathway, providing a potential candidate for CRC pre-diction and treatment.
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