Regulation of interleukin-8 expression in human prostate cancer cells by insulin-like growth factor-I and inflammatory cytokines

Kooijman, Ron; Himpe, Eddy; Potikanond, Saranyapin; Coppens, Astrid

doi:10.1016/j.ghir.2007.04.004

Cited by 16 publications

(20 citation statements)

References 54 publications

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“…IL-1β and TNF-α are reported to regulate IL-8 expression in fibroblasts (30), endothelial cells (31), gastric carcinoma (32) and prostate cancer (33). Soria et al (34) found that coordinated expression of TNF-α and IL-1β may promote breast cancer recurrence.…”

Section: Discussionmentioning

confidence: 99%

Macrophage-secreted IL-8 induces epithelial-mesenchymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway

Dai

Song

et al. 2014

International Journal of Oncology

191

147

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Abstract. Macrophages are a major component of the leukocyte infiltrate of tumors and play a pivotal role in the progression of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which macrophages promote HCC invasion are poorly understood. The present study was undertaken to investigate the relationship between macrophages and epithelial-mesenchymal transition (EMT) of HCC. Double-staining immunohistochemistry was used to observe the association between macrophages and EMT markers in clinical HCC samples and it showed that EMT primarily occurred at the edge of the tumor nest, in which infiltrating macrophages were always observed. This indicated that CD68 which is a marker of macrophages, was correlated with EMT marker levels. In addition, after being cultured with macrophages for 24 h, the ability of HCC cells to migrate and invade increased, Snail and N-Cadherin expression was upregulated, and E-Cadherin was downregulated. An antibody array assay was applied to analyze the supernatant of these cultures and it demonstrated IL-8 increased significantly in the macrophage co-culture system. Finally, the role of macrophage-derived IL-8 in the invasion of HCC cells was assayed, and downstream signaling pathways were also investigated. We found that IL-8: i) may induce EMT and promote HCC cell migration and invasion and ii) is associated with the JAK2/STAT3/Snail signaling pathway. Taking together, these findings revealed that macrophages that have infiltrated tumors may induce epithelial-mesenchymal transition of HCC cells via the IL-8 activated JAK2/STAT3/Snail pathway. Thus, this may offer a potential target for developing new HCC therapies.

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Section: Discussionmentioning

confidence: 99%

Macrophage-secreted IL-8 induces epithelial-mesenchymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway

Dai

Song

et al. 2014

International Journal of Oncology

191

147

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“…We recently reported that IGF-I augments the phosphorylation of the protein kinases Akt and Erk 1/2 in Du145 cells, while in PC3 and LNCaP cells only Akt became activated in the presence of IGF-I [14]. Possibly, both pathways are required for stimulation of DNA synthesis in prostate cancer cells and, in PC3 and LNCaP cells, IGF-I can only stimulate DNA synthesis in the presence of serum factors that activate the Mek-Erk pathway or other pathway(s).…”

Section: Signal Transduction Pathways Involved In Stimulation Of Dna mentioning

confidence: 99%

“…For instance, in vitro IGF-I increases the invasive capacity of Du145 cells [12], and the in vivo transition of LNCaP and LAPC9 cells to an androgen independence state, a less controllable cancer state, associates with IGF-I and IGF-I receptor levels [13]. We previously showed that IGF-I could increase IL8 expression [14], which has been associated with metastases and angiogenesis, partly due to up-regulation of metalloproteinase 9 (MMP-9) in prostate cancer [15]. Furthermore, two mouse models for prostate cancer associated with impaired GH production [16] or GH signaling [17] displayed reduced serum IGF-I levels and a decreased progression of prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of IGF-I receptor signaling inhibits serum-induced proliferation of prostate cancer cells

Himpe

Potikanond

Verdood

et al. 2011

Growth Hormone & IGF Research

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“…Although there is no doubt that LNCaP is androgen-sensitive, it is not completely androgen-dependent (5). If the androgen-dependent effects are investigated in LNCaP cells, this should be taken into account, and additional investigation may be required to claim that the effect is androgen-specific, e.g.…”

Section: The Pure Anti-androgen Bicalutamide Inhibits Cyclin a Expresmentioning

confidence: 99%

The pure anti-androgen bicalutamide inhibits cyclin A expression both in androgen-dependent and -independent cell lines

Katayama

Murashima²,

Saeki³

et al. 2010

Int J Oncol

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We investigated the effects of testosterone and the pure anti-androgen, bicalutamide, on DNA synthesis and cell cycle in androgen-sensitive or -insensitive human and mouse cell lines by 3 H-thymidine incorporation, flow cytometry, RT-PCR and Western blotting. In androgen-dependent mouse SC-3 cells, testosterone induced DNA synthesis, shift of cell cycle distribution from G0/G1 to S/G2/M and expression of cyclin A. The induction was preceded by that of fibroblast growth factor 8 (FGF-8), and completely blocked by monoclonal antibody to FGF-8. Dihydrotestosterone (DHT) induced cyclin A expression in androgen-sensitive human prostate cancer cells, but not in androgen-independent cell lines. Bicalutamide almost completely inhibited these androgen-dependent effects both in LNCaP and SC-3 cells, but had no or limited effect on androgen-independent or FGF-8-induced DNA synthesis, and FGF-8 induced cyclin A expression. Interestingly, bicalutamide inhibited both DNA synthesis and the cyclin A expression in androgenindependent human cell lines in serum-free condition. A MEK1/2 inhibitor U0126 blocked both androgen-and rFGF-8-induced DNA synthesis. Overall, bicalutamide inhibits the cyclin A expression possibly by inhibiting FGF-8 mRNA expression and FGF-8 protein secretion but not by inhibiting FGF receptor (FGFR) signalling in androgendependent cell lines, and by other mechanisms in androgenindependent cell lines. The results suggest that combination with compounds such as FGFR signalling inhibitors may provide additional benefits to anti-androgens. It is also suggested that cyclin A could be a sensitive marker for androgen-induced cancer growth and for the growth inhibitory effects of anti-androgen.

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Regulation of interleukin-8 expression in human prostate cancer cells by insulin-like growth factor-I and inflammatory cytokines

Cited by 16 publications

References 54 publications

Macrophage-secreted IL-8 induces epithelial-mesenchymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway

Macrophage-secreted IL-8 induces epithelial-mesenchymal transition in hepatocellular carcinoma cells by activating the JAK2/STAT3/Snail pathway

Attenuation of IGF-I receptor signaling inhibits serum-induced proliferation of prostate cancer cells

The pure anti-androgen bicalutamide inhibits cyclin A expression both in androgen-dependent and -independent cell lines

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