microRNA-26a suppresses recruitment of macrophages by down-regulating macrophage colony-stimulating factor expression through the PI3K/Akt pathway in hepatocellular carcinoma

被引:72
|
作者
Chai, Zong-Tao [1 ,2 ]
Zhu, Xiao-Dong [1 ,2 ]
Ao, Jian-Yang [1 ,2 ]
Wang, Wen-Quan [3 ,4 ,5 ]
Gao, Dong-Mei [1 ,2 ]
Kong, Jian [6 ]
Zhang, Ning [1 ,2 ]
Zhang, Yuan-Yuan [1 ,2 ]
Ye, Bo-Gen [1 ,2 ]
Ma, De-Ning [1 ,2 ]
Cai, Hao [1 ,2 ]
Sun, Hui-Chuan [1 ,2 ]
机构
[1] Fudan Univ, Zhongshan Hosp, Liver Canc Inst, Shanghai 200032, Peoples R China
[2] Fudan Univ, Minist Educ, Key Lab Carcinogenesis & Canc Invas, Shanghai 200032, Peoples R China
[3] Fudan Univ, Shanghai Canc Ctr, Dept Pancreat & Hepatobiliary Surg, Shanghai 200032, Peoples R China
[4] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China
[5] Fudan Univ, Pancreat Canc Inst, Shanghai 200032, Peoples R China
[6] Capital Med Univ, Beijing Chaoyang Hosp, Dept Hepatobiliary Surg, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
microRNA-26a; Hepatocellular carcinoma; M-CSF; Macrophages; TUMOR-ASSOCIATED MACROPHAGES; PERITUMORAL LIVER-TISSUE; ACTIVATED MONOCYTES; DISEASE PROGRESSION; VENOUS METASTASES; GROWTH; PROGNOSIS; APOPTOSIS; ACID; TUMORIGENICITY;
D O I
10.1186/s13045-015-0150-4
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: microRNAs (miRNAs) have been reported to modulate macrophage colony-stimulating factor (M-CSF) and macrophages. The aim of this study was to find whether miR-26a can suppress M-CSF expression and the recruitment of macrophages. Methods: Hepatocellular carcinoma (HCC) cell lines with decreased or increased expression of miR-26a were established in a previous study. M-CSF expression by tumor cells was measured by enzyme-linked immunosorbent assay, and cell migration assays were used to explore the effect of HCC cell lines on macrophage recruitment in vitro. Real-time PCR measured a panel of mRNAs expressed by macrophages. Xenograft models were used to observe tumor growth. Immunohistochemistry was conducted to study the relation between miR-26a expression and M-CSF expression and macrophage recruitment in patients with HCC. Results: Ectopic expression of miR-26a reduced expression of M-CSF. The conditioned medium (CM) from HepG2 cells that overexpressed miR-26a reduced the migration ability of THP-1 cells stimulated by phorbol myristate acetate (PMA) increased expression of interleukin (IL)-12b or IL-23 mRNA and decreased expression of chemokine (C-C motif) ligand (CCL) 22, CCL17, and IL-10 mRNA, in comparison to the medium from the parental HepG2 cells. These effects could be interrupted by the PI3K/Akt pathway inhibitor LY294002. Ectopic expression of miR-26a in HCC cells suppressed tumor growth, M-CSF expression, and infiltration of macrophages in tumors. Similar results were also found when using HCCLM3 cells. Furthermore, the expression of miR-26a was inversely correlated with M-CSF expression and macrophage infiltration in tumor tissues from patients with HCC. Conclusions: miR-26a expression reduced M-CSF expression and recruitment of macrophages in HCC.
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页数:11
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