Effect of serum deprivation on constitutive production of granulocyte‐colony stimulating factor and granulocyte macrophage‐colony stimulating factor in lung cancer cells

Uemura, Yoshiki; Kobayashi, Makoto; Nakata, Hideshi; Harada, Ryoji; Kubota, Tetsuya; Taguchi, Hirokuni

doi:10.1002/ijc.20023

Cited by 20 publications

(11 citation statements)

References 40 publications

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“…(36,37) CSF extend the life span of mature leukocytes by inhibiting their apoptotic death; this function may not be confined only to hematopoietic cells, but may extend also to cancer cells. (38,39) In the present study, it was observed that almost all lung cancer cell lines produced various kinds of cytokines. These cytokines seemed to have such functions as tumor progression, angiogenesis and an inhibition of the immune response.…”

Section: P-valuementioning

confidence: 52%

Cytokine production of lung cancer cell lines: Correlation between their production and the inflammatory/immunological responses both in vivo and in vitro

et al. 2007

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Cytokines produced by tumor cells may have various effects on antitumor immune responses and tumor growth. In the present study, the cytokine production of 31 lung cancer cell lines was evaluated, while any correlation with the histological type, the induction of tumor‐specific cytotoxic T lymphocytes (CTL) in vitro, and angiogenesis and the infiltration of inflammatory cells in tumor tissues were also examined. Production of interleukin (IL)‐1α, IL‐1β, IL‐4, IL‐6, IL‐8, IL‐10, tumor necrosis factor (TNF)‐α, granulocyte macrophage colony stimulating factor (GM‐CSF), granulocyte colony stimulating factor, transforming growth factor (TGF)‐β and vascular endothelial growth factor (VEGF) in the culture supernatant was measured using enzyme‐linked immunosorbent assay. Each cytokine was produced in a substantial number of the tumor cell lines. In particular, IL‐6, IL‐8, TGF‐β and VEGF were produced in 18 (55%), 29 (94%), 31 (100%) and 28 (90%) of 31 cell lines, respectively. However, neither IL‐4 nor TNF‐α was produced at all by any tumor cell line. TGF‐β production was significantly higher in adenocarcinoma than in squamous cell carcinoma (P = 0.03). Immunohistochemical staining revealed the magnitude of macrophage infiltration, and angiogenesis in surgically resected tumor tissue specimens correlated well with GM‐CSF and IL‐8 production from the corresponding cell lines. Among six lung cancer cell lines, CTL were induced in the three lung cancer cell lines that produced a lower amount of TGF‐β (<100 pg/mL). These findings suggested that TGF‐β produced by tumor cells could inhibit the induction of CTL in vitro. The present results suggest that the production of various cytokines from tumor cells might exert various paracrine effects both in vivo and in vitro. (Cancer Sci 2007; 98: 1048–1054)

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Section: P-valuementioning

confidence: 52%

Cytokine production of lung cancer cell lines: Correlation between their production and the inflammatory/immunological responses both in vivo and in vitro

et al. 2007

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“…Mroczko et al demonstrated that CSFs could be useful in diagnostics and monitoring of NSCLC (5). Some studies show that CSFs produced by lung cancer cells might promote tumor progression through an autocrine mechanism (6,7). Exogenous CSFs also promote invasion by lung cancer cells through the enhanced production of extracellular matrixdegrading proteinases by the tumor cells or prolong tumor cell survival (8,9).…”

Section: Introductionmentioning

confidence: 99%

Effects of GM-CSF and M-CSF on tumor progression of lung cancer: Roles of MEK1/ERK and AKT/PKB pathways

Uemura

Nakata²,

Kubota³

et al. 2006

Int J Mol Med

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Abstract. Several studies have demonstrated that colonystimulating factors (CSFs) are closely associated with tumor progression, metastasis and invasion through autocrine or paracrine mechanism in lung cancer. However, biologic roles of CSFs are still unknown. Elucidating the biologic roles of CSFs and the regulatory mechanisms of tumor-specific behavior by CSFs raises the possibility of having a new therapeutic approach for lung cancer. We previously established two adenocarcinoma cell lines, A924 and A964 and a large cell carcinoma cell line MI-4. MI-4 and A924 constitutively produced an abundant dose of granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF). We examined the effects of GM-CSF and M-CSF on tumor growth, death, and invasion in CSF-producing (A924 and MI-4) and non-producing lung cancer cells (A549 and A964). These cell lines demonstrated both GM-CSF and M-CSF receptor mRNA expression. In our study, GM-CSF seemed to have advantage for tumor proliferation and invasion in lung cancer cells. M-CSF seemed to have advantage for tumor invasion, but not proliferation. The tumor-specific phenotypes (proliferation, invasion and survival) up-regulated by GM-CSF and M-CSF were mediated through MEK/ERK and PI3k/Akt pathways. However, when MEK/ERK was activated by transfection of active form of MEK1 cDNA, the tumor-specific behavior was promoted in CSF-non-producing cells, whereas inhibited in CSF-producing cells though MEK/ERK activation increased constitutive GM-CSF production. MEK/ERK signaling regulated differently tumor-specific behavior between CSFproducing cells and CSF-non-producing cells.

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“…Several reports have demonstrated a MAPK-and NF-Bmediated autocrine growth loop for G-CSF in nonhematopoietic tumor cells in which serum deprivation stimulated constitutive production of G-CSF (21,36). Although known for some time to be proliferative for granulocytes and human endothelial cells (5,26), there is only one other report in the literature describing expression of G-CSF in human VSMC (34).…”

Section: Discussionmentioning

confidence: 96%

Expression of granulocyte colony-stimulating factor is induced in injured rat carotid arteries and mediates vascular smooth muscle cell migration

Xing¹,

Kelemen²,

Autieri³

2005

American Journal of Physiology-Cell Physiology

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Granulocyte colony-stimulating factor (G-CSF) is a lineage-restricted hematopoietic growth factor that stimulates proliferation and maturation of hematopoietic progenitors and is a known powerful mobilizer of bone marrow-derived stem cells. Very little has been reported on G-CSF expression and modulation of vascular smooth muscle cell (VSMC) activation. The purpose of this study was to characterize the expression and effects of G-CSF on primary human VSMC and balloon angioplasty-injured rat carotid arteries. In cultured human VSMC, G-CSF mRNA and protein expression are induced by several cytokines, with the most potent being fetal calf serum and T-lymphocyte-conditioned media. G-CSF is not expressed in naive rat carotid arteries but is induced in neointimal SMC in carotid arteries subject to balloon angioplasty. G-CSF is chemotactic for human VSMC. There is a significant difference between unstimulated cells and those treated with G-CSF at 100 and 1,000 pg/ml (P < 0.01 and 0.05 for 3 experiments). G-CSF also activates the GTPase Rac1, a regulator of cellular migration in VSMC. Inhibition of Rac1 inhibits G-CSF-driven VSMC migration. Important signal transduction protein kinases, including p44/42 MAPK, Akt, and S6 kinase, are also activated in response to G-CSF. This is the first report describing the expression of G-CSF in injured arteries and the multiple effects of G-CSF on VSMC activation. Together, our data suggest that G-CSF is an important mediator of inflammatory cell-VSMC communication and VSMC autocrine activation and may be an important mediator of the VSMC response to injury.

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Effect of serum deprivation on constitutive production of granulocyte‐colony stimulating factor and granulocyte macrophage‐colony stimulating factor in lung cancer cells

Cited by 20 publications

References 40 publications

Cytokine production of lung cancer cell lines: Correlation between their production and the inflammatory/immunological responses both in vivo and in vitro

Cytokine production of lung cancer cell lines: Correlation between their production and the inflammatory/immunological responses both in vivo and in vitro

Effects of GM-CSF and M-CSF on tumor progression of lung cancer: Roles of MEK1/ERK and AKT/PKB pathways

Expression of granulocyte colony-stimulating factor is induced in injured rat carotid arteries and mediates vascular smooth muscle cell migration

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