[Fatty acids regulate macrophage polarization to inhibit the growth and metastasis of lung cancer cells induced by intermittent hypoxia].

Effects of lipid metabolism on the polarization of macrophages and proliferation and migration of lung cancer cells under intermittent hypoxia. THP-1 cells were treated with 100 ng/mL PMA for 48h to induce differentiation into M0 macrophages, and 20 ng/mL IL-4 for 24 h to induce polarization of macrophages under normal oxygen or CIH environment. The expression levels of CD86, TNF-α, CD206 and IL-10 were detected by qRT-PCR. The mRNA levels of CD86, TNF-α, CD206 and IL-10 in macrophages were detected by qRT-PCR after the intervention of palmitic acid and arachidonic acid. A549 cells were co-cultured with supernatant and divided into normoxic control group (RA control), normoxic palmitic acid group (RA-PA), normoxic arachidonic acid group (RA-AA), CIH control group (CIH control), CIH-palmitic acid group (CIH-PA) and CIh-arachidonic acid group (CIH-AA). The proliferation rate of A549 cells was detected by CCK-8 method. Cell migration ability was detected by scratch test. The protein expression of MMP2 and MMP9 was detected by Western blot. The cell invasion ability was detected by Transwell assay. The expression levels of palmitic acid, arachidonic acid, TNF-α and IL-10 were detected by ELISA. In A549 cells, compared with the RA control group, the proliferation activity, migration and invasion ability of CIH control group were increased (＜0.05), the expressions of MMP2 and MMP9 protein and IL-10 were increased (＜0.05), and the expressions of palmitic acid, arachidonic acid and TNF-α were decreased (＜0.05). Compared with the CIH control group, the proliferation ability, migration and invasion ability of CIH-PA group and CIH-AA group were decreased (＜0.05), and the expression of MMP2 and MMP9 protein and IL-10 were decreased (＜0.05). The expressions of palmitic acid, arachidonic acid and TNF-α were increased (＜0.05). Palmitic acid and arachidonic acid reduce the proliferation, metastasis and invasion of lung cancer cells induced by CIH by inhibiting the M2-type polarization of macrophages.