Abstract:
Objective To investigate the Effects of entinostat on the expression of NKG2D ligands in the non- small cell lung cancer (NSCLC) cell lines, A549 and HCC-827, and to detect the effect of entinostat-mediated NK cell killing of A549 and HCC-827 cells.
Methods The effect of entinostat on A549 and HCC-827 cell proliferation was measured by MTT assay. Flow cytometry was used to detect the expression of NKG2D ligands. mRNA levels of the ligands were detected by RT-PCR. The level of soluble MICA in cell culture supernatant was evaluated by ELISA. The cytotoxicity of NK cells against A549 and HCC-827 cell lines (treated with entinostat) was assessed using lactate dehydrogenase release assay.
Results Entinostat showed a time- and dose-dependent inhibition effect on the proliferation of A549 and HCC-827 cell lines. The expression of NKG2D ligands and mRNA transcription levels of MICA and MICB were enhanced after treatment with 0.5, 1 μmol/L entinostat for 48 h. The soluble MICA level in A549 cell culture supernatant was increased by 1 μmol/L entinostat. The sensitivity of HCC-827 cells to NK cells was enhanced upon treatment with 0.5, 1 μmol/L entinostat.
Conclusions entinostat enhanced the killing effect of NK cells on non-small cell lung cancer cells by up-regulating the expression of NKG2D ligands. This provides a new method and theory for the treatment of NSCLC.
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