Role of JNK/ATF-2 pathway in inhibition of thrombospondin-1 (TSP-1) expression and apoptosis mediated by doxorubicin and camptothecin in FTC-133 cells

Btaouri, Hassan El; Morjani, Hamid; Greffe, Yannick; Charpentier, Emmanuelle; Martiny, Laurent

doi:10.1016/j.bbamcr.2011.02.004

Cited by 14 publications

(13 citation statements)

References 54 publications

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“…The antiapoptotic role of TSP-1 involves its C-terminal part that interacts with the membrane receptor CD47. More recently, we have shown that both doxorubicin was able to activate JNK/ATF-2 pathway to downregulate TSP-1 expression and to modulate apoptosis [40]. The role of TSP-1 in the protection of thyroid carcinoma cells will be discussed in more detail in this second part of the paper.…”

Section: Modulation Of Chemotherapy-induced Apoptosis By Extracellmentioning

confidence: 99%

Extracellular Matrix Proteins Modulate Antimigratory and Apoptotic Effects of Doxorubicin

Said

Guilbert

Morjani

et al. 2012

Chemotherapy Research and Practice

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Anticancer drug resistance is a multifactorial process that includes acquired and de novo drug resistances. Acquired resistance develops during treatment, while de novo resistance is the primary way for tumor cells to escape chemotherapy. Tumor microenvironment has been recently shown to be one of the important factors contributing to de novo resistance and called environment-mediated drug resistance (EMDR). Two forms of EMDR have been described: soluble factor-mediated drug resistance (SFM-DR) and cell adhesion-mediated drug resistance (CAM-DR). Anthracyclines, among the most potent chemotherapeutic agents, are widely used in clinics against hematopoietic and solid tumors. Their main mechanism of action relies on the inhibition of topoisomerase I and/or II and the induction of apoptosis. Beyond this well-known antitumor activity, it has been recently demonstrated that anthracyclines may display potent anti-invasive effects when used at subtoxic concentrations. In this paper, we will describe two particular modes of EMDR by which microenvironment may influence tumor-cell response to one of these anthracyclines, doxorubicin. The first one considers the influence of type I collagen on the antimigratory effect of doxorubicin (CAM-DR). The second considers the protection of tumor cells by thrombospondin-I against doxorubicin-induced apoptosis (SFM-DR).

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Section: Modulation Of Chemotherapy-induced Apoptosis By Extracellmentioning

confidence: 99%

Extracellular Matrix Proteins Modulate Antimigratory and Apoptotic Effects of Doxorubicin

Said

Guilbert

Morjani

et al. 2012

Chemotherapy Research and Practice

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“…Further, doxorubicin-induced cellular toxicity has been linked to increased ceramide synthesis, and inhibition of ceramide accumulation blocks the antineoplastic effects of this drug (23,24). Doxorubicin-induced HF has been associated with ceramide accumulation and apoptosis (20,25,26). Whether reduction of ceramide levels will improve late remodeling in HF has not been studied.…”

Section: Introductionmentioning

confidence: 99%

Increased de novo ceramide synthesis and accumulation in failing myocardium

Ji¹,

Akashi²,

Drosatos³

et al. 2017

JCI Insight

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Abnormal lipid metabolism may contribute to myocardial injury and remodeling. To determine whether accumulation of very long-chain ceramides occurs in human failing myocardium, we analyzed myocardial tissue and serum from patients with severe heart failure (HF) undergoing placement of left ventricular assist devices and controls. Lipidomic analysis revealed increased total and very long-chain ceramides in myocardium and serum of patients with advanced HF. After unloading, these changes showed partial reversibility. Following myocardial infarction (MI), serine palmitoyl transferase (SPT), the rate-limiting enzyme of the de novo pathway of ceramide synthesis, and ceramides were found increased. Blockade of SPT by the specific inhibitor myriocin reduced ceramide accumulation in ischemic cardiomyopathy and decreased C16, C24:1, and C24 ceramides. SPT inhibition also reduced ventricular remodeling, fibrosis, and macrophage content following MI. Further, genetic deletion of the SPTLC2 gene preserved cardiac function following MI. Finally, in vitro studies revealed that changes in ceramide synthesis are linked to hypoxia and inflammation. In conclusion, cardiac ceramides accumulate in the failing myocardium, and increased levels are detectable in circulation. Inhibition of de novo ceramide synthesis reduces cardiac remodeling. Thus, increased de novo ceramide synthesis contributes to progressive pathologic cardiac remodeling and dysfunction.

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“…Importantly, transcriptional repression is a common mechanism regulating the expression of TSP-1 – it results in a rapid effect, because both the protein and mRNA of TSP-1 are unstable (69, 70, 78, 100, 101). …”

Section: Introductionmentioning

confidence: 99%

Invoking the power of thrombospondins: Regulation of thrombospondins expression

Stenina‐Adognravi¹

2014

Matrix Biology

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Increasing evidence suggests critical functions of thrombospondins (TSPs) in a variety of physiological and pathological processes. With the growing understanding of the importance of these matricellular proteins, the need to understand the mechanisms of regulation of their expression and potential approaches to modulate their levels is also increasing. The regulation of TSPs expression is multi-leveled, cell- and tissue-specific, and very precise. However, the knowledge of mechanisms modulating the levels of TSPs is fragmented and incomplete. This review discusses the known mechanisms of regulation of TSPs levels and the gaps in our knowledge that prevent us from developing strategies to modulate the expression of these physiologically important proteins.

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Role of JNK/ATF-2 pathway in inhibition of thrombospondin-1 (TSP-1) expression and apoptosis mediated by doxorubicin and camptothecin in FTC-133 cells

Cited by 14 publications

References 54 publications

Extracellular Matrix Proteins Modulate Antimigratory and Apoptotic Effects of Doxorubicin

Extracellular Matrix Proteins Modulate Antimigratory and Apoptotic Effects of Doxorubicin

Increased de novo ceramide synthesis and accumulation in failing myocardium

Invoking the power of thrombospondins: Regulation of thrombospondins expression

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