Knockdown of long non-coding RNA MIR155HG suppresses melanoma cell proliferation, and deregulated MIR155HG in melanoma is associated with M1/M2 balance and macrophage infiltration

This study aimed to address the roles of long non-coding RNA (lncRNA) MIR155HG in melanoma cell proliferation and apoptosis, as well as the roles of deregulated MIR155HG in melanoma cells in regulation M1/M2 macrophage balance and macrophage infiltration. In this study, melanoma A375 and SK-MEL-28 cells that transfected with MIR155HG knockdown or overexpression plasmid were subjected to examinations of cell viability, colony formation ability, cell cycle distribution and apoptosis. Then, monocytic THP-1 cells were differentiated and polarized into M1 and M2 phenotypes. M1 and M2 markers were identified and MIR155HG levels in M0, M1 and M2 macrophages were determined. Next, conditioned medium (CM) from A375 cells knocking down or overexpressing MIR155HG was harvested to stimulate M0 macrophages. M1/M2 markers and macrophage infiltration were analyzed. The results showed that MIR155HG knockdown markedly reduced cell viability, suppressed colony formation, arrested the cell cycle at G1 phase and promoted apoptosis of A375 and SK-MEL-28 cells. Next, we successfully obtained and identified M1/M2 macrophages. Interestingly, M1 macrophages expressed lower, while M2 macrophages expressed higher levels of MIR155HG. More importantly, we also found that CM from A375 cells knocking down MIR155HG favored M1 polarization and ameliorated macrophage infiltration, while CM from MIR155HG overexpressing cells promoted M2 polarization and accelerated macrophage infiltration. These evidences suggest that MIR155HG knockdown may inhibit melanoma cell proliferation, aberrant MIR155HG levels correlate with the regulation of M1/M2 macrophage balance and macrophage infiltration in tumor microenvironment.