IFN-γ induces overexpression of PD-L1 and epithelialmesenchymal transformation of breast cancer cells through activating ERK/Jak2-STAT signaling pathways.
- Author:
Yurong YAN
1
;
Chenchen ZHAO
1
;
Rui YANG
1
;
Ting ZHOU
1
;
Na XU
1
Author Information
- Publication Type:Journal Article
- Keywords: ERK; IFN-γ; Jak2; PD-L1; breast cancer; epithelial-mesenchymal transition
- MeSH: B7-H1 Antigen; Breast Neoplasms; Cell Line, Tumor; Cell Movement; Epithelial-Mesenchymal Transition; Extracellular Signal-Regulated MAP Kinases; Humans; Interferon-gamma; Janus Kinase 2; STAT Transcription Factors; Signal Transduction
- From: Chinese Journal of Biotechnology 2018;34(12):2007-2015
- CountryChina
- Language:Chinese
- Abstract: To investigate the effect of INF-γ on the expression of programmed death ligand 1 (PD-L1), epithelial-mesenchymal transition (EMT) and the potential mechanism in breast cancer cell line MDA-MB-231, the cells were treated with different concentrations of INF-γ. The expressions of proteins, including PD-L1, cell-migration-related proteins (E-cadherin, N-cadherin and vimentin), ERK, p-ERK, Jak2, and p-Jak2 were detected by Western blotting analysis and immunofluorescent staining assay. Cell migration was studied through cell wound healing assay and transwell assay. IFN-γ could up-regulate the expressions of PD-L1 in MDA-MB-231 cells. The cell migration rate was significantly increased after adding IFN-γ. The expression levels of vimentin and N-cadherin were increased whereas the expression of E-cadherin was decreased after adding IFN-γ. The expression levels of ERK, p-ERK, Jak2 and p-Jak2 were significantly increased and this phenomenon was inhibited when adding ERK inhibitor U0126 or Jak2 inhibitor AG490. These results demonstrate that IFN-γ could up-regulate the expression of PD-L1, promote cell migration and transmission, and facilitate epithelial-mesenchymal transformation of breast cancer cells and this process may be related with ERK and Jak2-STAT signaling pathways.
