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MiR-98 modulates macrophage polarization and suppresses the effects of
tumor-associated macrophages on promoting invasion and epithelial-mesenchymal
transition of hepatocellular carcinoma
#MMPMID29989015
Li L
; Sun P
; Zhang C
; Li Z
; Cui K
; Zhou W
Cancer Cell Int
2018[]; 18
(?): 95
PMID29989015
show ga
BACKGROUND: Tumor-associated macrophages (TAMs) are generally recognized as a
promoter of tumor progression. miR-98 has been shown to suppress the
proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of
hepatocellular carcinoma (HCC) cells. Here, we aim to investigate the role of
miR-98-mediated macrophage polarization in HCC progression. METHODS: Human blood
monocytes were isolated from healthy male donors and incubated with culture
medium collected from HepG2 cells for 7 days. The phenotype of the macrophages
was detected. The protein expression was detected by Western blot. Levels of
cytokines secreted in culture medium were measured using the specific
enzyme-linked immunosorbent assay kits. To explore the role of miR-98 in
HCC-conditioned TAMs, HCC cells HepG2 and SMMC7721 were cultured with conditioned
medium from HCC-conditioned TAMs that had been transfected with miR-98
mimic/inhibitor. Cell proliferation, migration and invasion assays were
performed. RESULTS: HCC-conditioned TAMs possessed M2-like phenotype, including
increased protein expression of CD163 and TNF-?(low), IL-1?(low), TGF-?(high) and
IL-10(high) phenotype. HCC-conditioned TAMs also promoted proliferation,
migration, invasion and EMT of HepG2 and SMMC7721 cells. Furthermore, miR-98
modulated macrophage polarization from M2 to M1 in HCC-conditioned TAMs, as
evidenced by the alteration of M1- or M2-related cytokines. Moreover, miR-98
mimic significantly suppressed the HCC-conditioned TAMs-mediated promotion of
cell migration, invasion and EMT in HepG2 and SMMC7721 cells compared with
negative control, whereas miR-98 inhibitor exerted reversed effects. CONCLUSIONS:
miR-98 may play a vital role in regulating macrophage polarization, thereby
suppressing the TAMs-mediated promotion of invasion and EMT in HCC.
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