The effect of thalidomide on non-small cell lung cancer (NSCLC) cell lines: possible involvement in the PPAR  pathway

DeCicco, Kathleen L.

doi:10.1093/carcin/bgh210

Cited by 27 publications

(20 citation statements)

References 27 publications

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“…With regard to peroxisome proliferation PPARα is currently the best-studied PPAR whilst the precise role of the other PPARs is less well-defined [33,36]. Several studies have implicated PPARβ and PPARγ as playing a role in a variety of different systems but how this is related to peroxisome proliferation is not clear.…”

Section: Other Ppar Family Membersmentioning

confidence: 99%

Proliferation and fission of peroxisomes — An update

Schrader

Costello

Godinho

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

124

142

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In mammals, peroxisomes perform crucial functions in cellular metabolism, signalling and viral defense which are essential to the health and viability of the organism. In order to achieve this functional versatility peroxisomes dynamically respond to molecular cues triggered by changes in the cellular environment. Such changes elicit a corresponding response in peroxisomes, which manifests itself as a change in peroxisome number, altered enzyme levels and adaptations to the peroxisomal structure. In mammals the generation of new peroxisomes is a complex process which has clear analogies to mitochondria, with both sharing the same division machinery and undergoing a similar division process. How the regulation of this division process is integrated into the cell's response to different stimuli, the signalling pathways and factors involved, remains somewhat unclear. Here, we discuss the mechanism of peroxisomal fission, the contributions of the various division factors and examine the potential impact of post-translational modifications, such as phosphorylation, on the proliferation process. We also summarize the signalling process and highlight the most recent data linking signalling pathways with peroxisome proliferation.

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Section: Other Ppar Family Membersmentioning

confidence: 99%

Proliferation and fission of peroxisomes — An update

Schrader

Costello

Godinho

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

124

142

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“…1C). For comparison, cytokines that have been found to be overexpressed in lung cancer cell lines, including CXCL1, CXCL5, and IL-8 (17,18), showed no apparent regulatory effects on the phenotype of MdDC (Supplemental Fig. 1D).…”

Section: Galectin-1 Is Expressed Differently In Lung Cancer Cell Linementioning

confidence: 99%

Lung Cancer-Derived Galectin-1 Mediates Dendritic Cell Anergy through Inhibitor of DNA Binding 3/IL-10 Signaling Pathway

Kuo

Hung

Huang

et al. 2011

The Journal of Immunology

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Lung cancer, one of the leading causes of death worldwide, is often associated with a state of immune suppression, but the molecular and functional basis remains enigmatic. Evidence is provided in this paper supporting the role of lung cancer-derived soluble lectin, galectin-1, as a culprit in dendritic cell (DC) anergy. We have shown that galectin-1 is highly expressed in lung cancer cell lines, together with the serum and surgical samples from lung cancer patients. Functionally, lung cancer-derived galectin-1 has been shown to alter the phenotypes of monocyte-derived DCs (MdDCs) and impair alloreactive T cell response, concomitant with the increase of CD4+CD25+FOXP3+ regulatory T cells. The regulatory effect of galectin-1 is mediated, in part, through its ability to induce, in an Id3 (inhibitor of DNA binding 3)-dependent manner, the expression of IL-10 in monocytes and MdDCs. This effect is inhibited by the addition of lactose, which normalizes the phenotypic and functional alterations seen in MdDCs. Of note, significant upregulation of IL-10 was seen in tumor-infiltrating CD11c+ DCs in human lung cancer samples. This was also noted in mice transplanted with lung cancer cells, but not in those receiving tumor cells with galectin-1 knockdown. Furthermore, a significant reduction was noted in lung cancer incidence and in the levels of IL-10–expressing, tumor-infiltrating DCs, in mice receiving galectin-1–silenced tumor cells. These results thus suggest that the galectin-1/IL-10 functional axis may be crucial in lung cancer-mediated immune suppression, and that galectin-1 may serve as a target in the development of lung cancer immunotherapy.

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“…Its high mortality and poor prognosis are due to the difficulty of early diagnosis, and high potential to invade locally and metastasize to distant organ (1). Despite advances in surgery, chemotherapy, and radiotherapy, survival benefits remains poor (2).…”

mentioning

confidence: 99%

A Novel Anticancer Effect of Thalidomide: Inhibition of Intercellular Adhesion Molecule-1–Mediated Cell Invasion and Metastasis through Suppression of Nuclear Factor-κB

Lin

Shun²,

et al. 2006

Clinical Cancer Research

127

103

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Purpose: Thalidomide has been reported to have antiangiogenic and antimetastatic effects.Intercellular adhesion molecule-1 (ICAM-1) was shown to be involved in monocyte adherence to epithelial cells and cancer cell invasion. In this study, we further investigated the role of ICAM-1 in tumorigenesis, including tumor formation and metastasis. ICAM-1 as a molecular target for cancer and the anticancer effect of thalidomide were investigated. Experimental Design: Expression of ICAM-1 protein in human lung cancer specimens was assessed by immunohistochemistry. ICAM-1 overexpressing A549 cells (A549/ICAM-1) were established to investigate the direct effect of ICAM-1 on in vitro cell invasion and in vivo tumor metastasis. Transient transfection and luciferase assay, electrophoretic mobility shift assay, and chromatin immunoprecipitation were done to assess the activity and binding of nuclear factor-nB to the ICAM-1 promoter. A xenograft model in nude mice was conducted to evaluate the anticancer effect of thalidomide. Results: High expression of ICAM-1 in human lung cancer specimens was correlated with a greater risk of advanced cancers (stages III and IV). A549/ICAM-1 cells were shown to induce in vitro cell invasion and in vivo tumor metastasis. Anti-ICAM-1 antibody and thalidomide had inhibitory effect on these events. Thalidomide also suppressed tumor necrosis factor-a^induced ICAM-1 expression through inhibition of nuclear factor-nB binding to the ICAM-1 promoter. The in vivo xenograft model showed the effectiveness of thalidomide on tumor formation. Conclusion: These studies provide a framework for targeting ICAM-1 as a biologically based therapy for cancer, and thalidomide might be effective in human lung cancer.

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The effect of thalidomide on non-small cell lung cancer (NSCLC) cell lines: possible involvement in the PPAR pathway

Cited by 27 publications

References 27 publications

Proliferation and fission of peroxisomes — An update

Proliferation and fission of peroxisomes — An update

Lung Cancer-Derived Galectin-1 Mediates Dendritic Cell Anergy through Inhibitor of DNA Binding 3/IL-10 Signaling Pathway

A Novel Anticancer Effect of Thalidomide: Inhibition of Intercellular Adhesion Molecule-1–Mediated Cell Invasion and Metastasis through Suppression of Nuclear Factor-κB

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