CCL2-CCL5/CCR4 contributed to radiation-induced epithelial-mesenchymal transition of HPAEpiC cells via the ERK signaling pathways.

ABSTRACT: Radiation-induced lung toxicity, including radiation pneumonitis and pulmonary fibrosis, often occurs in patients receiving radiation therapy. Epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AECs) plays critical roles in radiation-induced lung toxicity. In the present study, RNA sequencing was applied to examine the whole transcriptomes of human pulmonary AEC cells (HPAEpiC) with or without radiation treatment. We found that cytokine, chemokine and cell adhesion signaling pathways were enriched in radiation-treated cells. CCL2 (C-C Motif Chemokine Ligand 2), CCL5 and CCR4 (C-C Motif Chemokine Receptor 4) were among the top enriched genes in chemokine signaling pathway. The upregulation of CCL2, CCL5 and CCR4 in response to irradiation was confirmed at both mRNA and pr

SUBMITTER: Zhong Y 

PROVIDER: S-EPMC6413271 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature