Enhanced invasion of lung adenocarcinoma cells after co-culture with THP-1-derived macrophages via the induction of EMT by IL-6

Dehai, Che; Pan, Bo; Tian, Qiang; Lihua, Shang; Liu, Fang; Shi, Jin; Cao, Jingyan; Yu, Yan; Wang, Guangbin; Zhenjun, Yuan

doi:10.1016/j.imlet.2014.03.004

Cited by 69 publications

(62 citation statements)

References 35 publications

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“…Co-culture with the induced M2 macrophages was shown to be able to significantly promote the migration and invasion of ESCC cells, inducing EMT process, which was highly consistent with previous relevant findings. 7,17 However, it should be noted that we did not observe the direct evidence that M2 macrophages promoted proliferation of ESCC cells in vitro co-culture system, which was somewhat in disagreement with several previous reports reporting that M2 macrophages were found to be able to promote the growth of cancer cells. [18][19][20] The potential reason leading to the discrepant observation was unknown but it may be likely due to the different sensitivities of the techniques used for detection of proliferatory variation.…”

Section: Discussioncontrasting

confidence: 99%

IL‐1β from M2 macrophages promotes migration and invasion of ESCC cells enhancing epithelial‐mesenchymal transition and activating NF‐κB signaling pathway

Zhou

Zheng

Liu

et al. 2018

J of Cellular Biochemistry

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Despite the phenotype has been established that M2 macrophages promotes the metastasis of ESCC, question still remains as to how the M2 macrophages facilitated metastasis of ESCC cells. To begin with, immunohistochemistry was performed to detect the expression of CD163, one typical surface marker of M2 macrophages in 90 paired ESCC and its normal controls after meta-analyzing the relevant studies regarding M2 macrophages in ESCC, confirming that infiltration of M2 macrophages was significantly linked with lymph node metastasis, T classification, and inferior overall survival of ESCC. To explore the mechanism behind, protein factors secreted by M2 macrophages were identified using antibody microarray. Six different significantly differential protein factors were screened out, including IL-1β, TIMP1, IL-1α, MDC, TGF-β1, and TGF-β2. Among which, IL-1β was picked up as cytokine as interest based on previous reports and its absolute fold. Functional analysis of IL-1β showed that IL-1β was able to promote migration and invasion of ESCC cells, enhancing epithelial-mesenchymal transition, and activating NF-κB pathway. Our study supports the promoting role of M2 macrophages in metastasis of ESCC cells, enriching the profile of protein factors released from M2 macrophages.

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Section: Discussioncontrasting

confidence: 99%

IL‐1β from M2 macrophages promotes migration and invasion of ESCC cells enhancing epithelial‐mesenchymal transition and activating NF‐κB signaling pathway

Zhou

Zheng

Liu

et al. 2018

J of Cellular Biochemistry

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“…Previous reports showed that IL-6 could induce EMT in breast cancer, pancreatic cancer, and lung cancer [52][53][54]. In the present study, we verified that IL-6 is an autocrine factor that promotes EMT of ICC cells.…”

Section: Discussionsupporting

confidence: 86%

FXR Acts as a Metastasis Suppressor in Intrahepatic Cholangiocarcinoma by Inhibiting IL-6-Induced Epithelial-Mesenchymal Transition

Tang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Intrahepatic cholangiocarcinoma (ICC) is a complicated condition, with difficult diagnosis and poor prognosis. The expression and clinical significance of the farnesoid X receptor (FXR), an endogenous receptor of bile acids, in ICC is not well understood. Methods: Western blotting and immunochemical analyses were used to determine the levels of FXR in 4 cholangiocarcinoma cell lines, a human intrahepatic biliary epithelial cell line (HIBEpic) and 322 ICC specimens, respectively, while quantitative reverse transcription polymerase chain reaction was used to detect the mRNA levels of FXR in cholangiocarcinoma cell lines. We evaluated the prognostic value of FXR expression and its association with clinical parameters. We determined the biological significance of FXR in ICC cell lines by agonist-mediated activation and lentivirus-mediated silence. IL-6 expression was tested by an enzyme-linked immunosorbent assay and flow cytometry. In vitro, cell proliferation was examined by Cell Counting Kit-8, migration and invasion were examined by wound healing and transwell assays; in vivo, tumor migration and invasion were explored in NOD-SCID mice. Results: FXR was downregulated in ICC cell lines and clinical ICC specimens. Loss of FXR was markedly correlated with aggressive tumor phenotypes and poor prognosis in patients with ICC. Moreover, FXR expression also had significant prognostic value in carbohydrate antigen 19-9 (CA19-9) negative patients. The expression of FXR was negatively correlated with IL-6 levels in clinical ICC tissues. FXR inhibited the proliferation, migration, invasion and epithelial mesenchymal transition (EMT) of ICC cells via suppression of IL-6 in vitro. Obeticholic acid, an agonist of FXR, inhibited IL-6 production, tumor growth and lung metastasis of ICC in vivo. Conclusions: FXR could be a promising ICC prognostic biomarker, especially in CA19-9 negative patients with ICC. FXR inhibits the tumor growth and metastasis of ICC via IL-6 suppression.

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“…To test whether the expression level of AEG-1 can affect macrophage polarization, RT-QPCR assay was conducted to determine the expression levels of Interleukin 12 (IL-12) and TNF-α, M1 (activated macrophages) markers and Interleukin 10 (IL-10) and transforming growth factor-β (TGF-β), M2 (alternatively activated macrophages) markers [19]. There was no significant difference in the expression level of IL-12, TGF-β, and IL-10 between Mac-AEG-1 and Mac-vector (Figure 4A).…”

Section: Resultsmentioning

confidence: 99%

Elevated AEG-1 expression in macrophages promotes hypopharyngeal cancer invasion through the STAT3-MMP-9 signaling pathway

Liu

Zou

et al. 2016

Oncotarget

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Macrophages play a critical role in tumor invasion and metastasis, which remain major causes of mortality in patients with hypopharyngeal cancer. Here we investigate the effect of an oncogene, AEG-1 expressed in macrophages on the invasion of hypopharyngeal cancer cells. AEG-1 is more highly expressed in macrophages of human hypopharyngeal cancer samples compared with adjacent non-tumor controls. Using matrigel invasion assay system, THP-1-derived macrophages with forced AEG-1 overexpression enhance FaDu cell invasion whereas macrophages with AEG-1 silence inhibit. Matrix metalloproteinase 9 (MMP-9), which is important in tumor invasion and metastasis through degrading extracellular matrix, is up-reulated by AEG-1 partly through NF-κB p65 in macrophages. Intriguingly, macrophage AEG-1 also induces MMP-9 up-regulated expression in FaDu cells. Furthermore, macrophage AEG-1 activates signal transducer and activator of transcription 3 (STAT3) in FaDu cells, which is responsible for macrophage AEG-1-induced an increase in MMP-9 expression and invasion of FaDu cells. This is the first to demonstrate that macrophage AEG-1 promotes tumor invasion through up-regulation of MMP-9 in both macrophages and cancer cells. Thus, the results provide evidences that macrophage AEG-1 contributes to promotion of tumor invasion, and represents as a potential target in hypopharyngeal cancer therapy.

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Enhanced invasion of lung adenocarcinoma cells after co-culture with THP-1-derived macrophages via the induction of EMT by IL-6

Cited by 69 publications

References 35 publications

IL‐1β from M2 macrophages promotes migration and invasion of ESCC cells enhancing epithelial‐mesenchymal transition and activating NF‐κB signaling pathway

IL‐1β from M2 macrophages promotes migration and invasion of ESCC cells enhancing epithelial‐mesenchymal transition and activating NF‐κB signaling pathway

FXR Acts as a Metastasis Suppressor in Intrahepatic Cholangiocarcinoma by Inhibiting IL-6-Induced Epithelial-Mesenchymal Transition

Elevated AEG-1 expression in macrophages promotes hypopharyngeal cancer invasion through the STAT3-MMP-9 signaling pathway

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