Effects of Interferons and Tumour Necrosis Factor-α on Human Lung Cancer Cell Lines and the Development of an Interferon-Resistant Lung Cancer Cell Line

Pestana, E. Suarez; Björklund, G.; Larsson, Rolf; Nygren, Peter; Nilsson, Kenneth; Bergh, Jonas

doi:10.3109/02841869609109925

Cited by 5 publications

(2 citation statements)

References 21 publications

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“…IL-6 has been shown to inhibit growth and enhance motility in breast cancer cell lines (16). TNF-α has an antitumor effect in murine tumors and human tumor xenografts in vivo and appears to be cytotoxic to many human tumor cell lines in vitro (17). TGF-β is an important suppressor of primary tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

Induction of cytokines and growth factors by rapamycin in the microenvironment of brain metastases of lung cancer

et al. 2013

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The association between rapamycin and astrocytes in a tumor-bearing mouse model with brain metastases of non-small cell lung cancer (NSCLC) was investigated. For in vitro experiments, NCI-H358, a human lung adenocarcinoma cell line, was co-cultured with immortalized astrocytes, and treated with rapamycin, an mTOR inhibitor. We evaluated the expression of interleukin-1 (IL-1), interleukin-3 (IL-3), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF), chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1) in tumor cells in vivo. Rapamycin is cytotoxic in vitro; however, co-culturing tumor cells and astrocytes induced tumor cell survival. IL-1, IL-3, IL-6, TNF-α, TGF-β, PDGF, MCP-1 and MIP-1 expression were higher in rapamycin-treated mice compared to the control group, however, IGF-1 expression was lower. Notably, treatment with rapamycin before inoculating tumor cells affected cytokine expression in the tumor microenvironment. We suggest that growth factors and cytokines in the tumor microenvironment play a role in the survival of cancer cells in brain metastases.

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Section: Discussionmentioning

confidence: 99%

Induction of cytokines and growth factors by rapamycin in the microenvironment of brain metastases of lung cancer

et al. 2013

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“…The mechanisms of IFN resistance have been investigated by many researchers using IFN‐resistant cell lines. Loss of receptor expression and function was shown to be responsible for IFN resistance in H82 (human lung cancer cell line) [15], Capan 2 (human pancreatic carcinoma cell line) [16], and IFN‐resistant variants of Daudi and HeLa [17]. In addition, defects in the expression and activation of STAT1 and STAT2 were reported to be a major cause of IFN resistance in some cell lines [17–19].…”

Section: Discussionmentioning

confidence: 99%

Defective binding of IRFs to the initiator element of interleukin‐1β‐converting enzyme (ICE) promoter in an interferon‐resistant Daudi subline

et al. 1999

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All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

Manna

Aggarwal

2000

Oncogene

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Retinoids modulate the growth and dierentiation eects of TNF but the mechanism is not understood. In this study, we investigated the eect of all-trans-retinoic acid (ATRA) on the cell surface expression of TNF receptors and receptor-mediated signaling in various human lung cancer cell lines. ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the speci®c binding of 125 Ilabeled TNF to these cells, in a dose-and time-dependent manner. Treatment with 2 mM ATRA for 24 h at 378C produced the maximal increase. Scatchard analysis indicated that the increase induced by ATRA was due to an increase in receptor number and not to an increase in anity. The upmodulation of TNF receptors was also con®rmed by covalent receptor-ligand cross-linking studies. The increase in TNF receptors sensitized H596 cells to TNF-induced activation of NF-kB, AP-1 and apoptosis. A549 cells, however, were completely resistant to TNF-induced activation of NF-kB, AP-1 and apoptosis. Treatment of these cells with as little as 0.5 mM ATRA was eective in converting TNF-resistant cells to TNF-sensitive. Overall our results indicate that ATRA induces the TNF receptors in human lung cancer cells, which sensitizes them to TNF-induced signaling leading to activation of NF-kB, AP-1 and apoptosis.

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Effects of Interferons and Tumour Necrosis Factor-α on Human Lung Cancer Cell Lines and the Development of an Interferon-Resistant Lung Cancer Cell Line

Cited by 5 publications

References 21 publications

Induction of cytokines and growth factors by rapamycin in the microenvironment of brain metastases of lung cancer

Induction of cytokines and growth factors by rapamycin in the microenvironment of brain metastases of lung cancer

Defective binding of IRFs to the initiator element of interleukin‐1β‐converting enzyme (ICE) promoter in an interferon‐resistant Daudi subline

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

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