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. 2019 Sep 20;11(10):2264. doi: 10.3390/nu11102264

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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PG2 negatively modulates the secretion of tumor-promoting anti-inflammatory cytokines and inhibits the M2-MCM-induced cancer stem cell-like phenotype of NSCLC cells. (A) Western blot showing a dose-related up-regulation of CD80 and down-regulation of CD206 protein expressions in MDMs after PG2 treatment. (B) Representative histogram of ELISA result showing PG2 significantly inhibited IL-10-enhanced M2 macrophage proliferation and CCCM-cultivated M2 population, compared to the untreated control group. ELISA histogram showing that 16 mg/mL PG2 exposure significantly reversed the CCCM-enhanced (C) IL-10 and (D) IL-6 secretion by M2 cells. (E) Photo (upper panel) and graphical (lower panel) images showing that H441 and H1299 cells co-cultured with M1-MCM remained adherent, while M2-MCM co-cultured cells acquired an adhesion-independent cancer stem cell (CSC) phenotype. (F) PG2 inhibited the viability of tumorspheres grown from M2/H1299 co-culture in a dose-dependent manner. *p < 0.05, **p < 0.01, ***p < 0.001; β-actin served as loading control.