EZH2 enhances expression of CCL5 to promote recruitment of macrophages and invasion in lung cancer
| Autor: | Lei Zhang, Jing Luo, Lilong Xia, Guoping Chen, Xinhai Zhu, Yanhui Xu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0106 biological sciences
Chemokine Lung Neoplasms Biomedical Engineering Bioengineering chemokines macromolecular substances 01 natural sciences Applied Microbiology and Biotechnology CCL5 Metastasis 03 medical and health sciences macrophage recruitment 010608 biotechnology Drug Discovery medicine metastasis Humans Enhancer of Zeste Homolog 2 Protein Neoplasm Invasiveness EZH2 Lung cancer Chemokine CCL5 030304 developmental biology 0303 health sciences Gene knockdown biology Chemistry Process Chemistry and Technology Chemotaxis Macrophages Cell migration General Medicine Original Articles medicine.disease Neoplasm Proteins Gene Expression Regulation Neoplastic lung cancer Tumor progression A549 Cells Cancer research biology.protein Molecular Medicine Original Article Biotechnology |
| Zdroj: | Biotechnology and Applied Biochemistry |
| ISSN: | 1470-8744 0885-4513 |
| Popis: | EZH2 (enhancer of zeste homolog 2) regulates epigenetic gene silencing and functions as critical regulators in various tumor progression. Macrophages infiltration promotes cancer development via stimulating tumor cell migration and invasion. However, the effect of EZH2 on macrophages infiltration, cell invasion, and migration of lung cancer remains to be investigated. In this study, we found that knockdown of EZH2 inhibited macrophages chemotaxis and decreased chemokine ligand 5 (CCL5). Wound‐healing and transwell assays results showed that migration and invasion of lung cancer cells was inhibited by EZH2 deletion. Moreover, EZH2 overexpression increased CCL5 expression. Loss‐of functional assay indicated that the promotion ability of EZH2 on macrophages chemotaxis was inhibited by CCL5 knockdown. Mechanistically, the promotion ability of EZH2 on cell migration and invasion of lung cancer was also inhibited by CCL5 knockdown. The in vivo subcutaneous xenotransplanted tumor model also revealed that silence of EZH2 suppressed lung cancer metastasis and macrophages infiltration via regulation of CCL5. In conclusion, our findings indicated that EZH2 promoted lung cancer metastasis and macrophages infiltration via upregulation of CCL5, which might be the underlying mechanism of EZH2‐induced lung cancer cell progression. xxxx |
| Databáze: | OpenAIRE |
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