The Matrix Metalloproteinase Inhibitor Prinomastat Enhances Photodynamic Therapy Responsiveness in a Mouse Tumor Model

Ferrario, Angela; Chantrain, Christophe; Tiehl, Karl von; Buckley, Sue; Rucker, Natalie; Shalinsky, David R.; Shimada, Hiroyuki; DeClerck, Yves A.; Gomer, Charles J.

doi:10.1158/0008-5472.can-04-0071

Cited by 115 publications

(127 citation statements)

References 23 publications

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“…Interestingly, PDT increased the expression and activation of MMP-1, -3, -8 and -9 in BA tumors subjected to PDT with Photofrin, and also changed the expression of MMP regulators. In particular, there was an up-regulation in EMMPRIN levels, a protein that efficiently stimulates the production of MMPs [276], and a decrease of TIMP-1 expression, a protein that regulates the metabolism of the extracellular matrix [275,277]. Taken together, these findings indicate that a combination therapy approach, using PDT together with MMP inhibitors and/or antiangiogenic compounds, can increase the therapeutic efficacy.…”

Section: Regulators Of Angiogenesismentioning

confidence: 78%

“…Both peptides decreased VEGF expression and improved tumoricidal responses in PDTtreated BA mammary carcinoma tumors growing in C3H mice [271]. In this model, a synthetic inhibitor of matrix metalloproteinases (MMP), Prinomastat, also increased the percentage of long-term cures after photosensitization with Photofrin [275]. Interestingly, PDT increased the expression and activation of MMP-1, -3, -8 and -9 in BA tumors subjected to PDT with Photofrin, and also changed the expression of MMP regulators.…”

Section: Regulators Of Angiogenesismentioning

confidence: 99%

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Intracellular signaling mechanisms in photodynamic therapy

Almeida

Manadas

Carvalho

et al. 2004

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

242

292

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In photodynamic therapy (PDT) a sensitizer, light and oxygen are used to induce death of tumor cells and in the treatment of certain noncancerous conditions. Cell death in PDT may occur by apoptosis or by necrosis, depending on the sensitizer, on the PDT dose and on the cell genotype. Some sensitizers that have been used in PDT are accumulated in the mitochondria, and this may explain their efficiency in inducing apoptotic cell death, both in vitro and in vivo. In this review we will focus on the events that characterize apoptotic death in PDT and on the intracellular signaling events that are set in motion in photosensitized cells. Activation of phospholipases, changes in ceramide metabolism, a rise in the cytosolic free Ca 2 + concentration, stimulation of nitric oxide synthase (NOS), changes in protein phosphorylation and alterations in the activity of transcription factors and on gene expression have all been observed in PDT-treated cells. Although many of these metabolic reactions contribute to the demise process, some of them may antagonize cell death. Understanding the signaling mechanisms in PDT may provide means to modulate the PDT effects at the molecular level and potentiate its antitumor effectiveness. D

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Section: Regulators Of Angiogenesismentioning

confidence: 78%

Section: Regulators Of Angiogenesismentioning

confidence: 99%

Intracellular signaling mechanisms in photodynamic therapy

Almeida

Manadas

Carvalho

et al. 2004

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

242

292

View full text Add to dashboard Cite

show abstract

“…In our experimental model, gelatin zymography applied to tumor homogenates revealed the induction of an enzymatically active form of MMP-2 after ZnTMPP and 5-ALA PDT. It is well known that MMPs are synthesized in a latent form and are transformed to biologically active proteases under the influence of some cytokines, growth factors, oncogenes, or ROS (9). It was shown that the production of ROS induces the activation of proMMP-2 (35).…”

Section: Discussionmentioning

confidence: 99%

“…This process involves macrophages and/or the dendritic cells from the tumor, pro-inflammatory cytokines, chemokines (interleukin-1ß (IL-1ß), tumor necrosis factor-alpha (TNF-α), IL-6, inflammatory proteins from the macrophage (MIP-1, MIP-2), and adhesion molecules (2,7). The pro-inflammatory cytokines and ROS activate the matrix metalloproteases (MMPs), which are proteolytic enzymes involved in the degradation of the extracellular matrix and also in invasion, angiogenesis, and metastasis (8,9).…”

Section: Introductionmentioning

confidence: 99%

Possible in vivo mechanisms involved in photodynamic therapy using tetrapyrrolic macrocycles

Filip

Clichici

Daicoviciu

et al. 2011

Braz J Med Biol Res

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“…Thus, induction of collagen-degrading enzymes together with a reduction of collagen production was thought to be responsible for the antisclerotic effects of ALA-PDT observed in vivo (55). PDT can also increase both the expression and the enzymatic activity of MMP-9 in BA tumors (56). The inflammatory response and host cell infiltration, described previously, suggest that the increased expression of MMP-9 observed in tumor tissue after PDT involves the influx of MMP-9-expressing inflammatory host cells, as opposed to direct PDTinduced expression of MMP-9 in inflammatory cells present within tumor tissue at the time of treatment.…”

Section: Matrix Metalloproteinasementioning

confidence: 99%

Effect of photodynamic therapy on the extracellular matrix and associated components

Pazos

Nader

2007

Braz J Med Biol Res

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In many countries, photodynamic therapy (PDT) has been recognized as a standard treatment for malignant conditions (for example, esophageal and lung cancers) and non-malignant ones such as age-related macular degeneration and actinic keratoses. The administration of a non-toxic photosensitizer, its selective retention in highly proliferating cells and the later activation of this molecule by light to form reactive oxygen species that cause cell death is the principle of PDT. Three important mechanisms are responsible for the PDT effectiveness: a) direct tumor cell kill; b) damage of the tumor vasculature; c) post-treatment immunological response associated with the leukocyte stimulation and release of many inflammatory mediators like cytokines, growth factors, components of the complement system, acute phase proteins, and other immunoregulators. Due to the potential applications of this therapy, many studies have been reported regarding the effect of the treatment on cell survival/death, cell proliferation, matrix assembly, proteases and inhibitors, among others. Studies have demonstrated that PDT alters the extracellular matrix profoundly. For example, PDT induces collagen matrix changes, including cross-linking. The extracellular matrix is vital for tissue organization in multicellular organisms. In cooperation with growth factors and cytokines, it provides cells with key signals in a variety of physiological and pathological processes, for example, adhesion/migration and cell proliferation/differentiation/death. Thus, the focus of the present paper is related to the effects of PDT observed on the extracellular matrix and on the molecules associated with it, such as, adhesion molecules, matrix metalloproteinases, growth factors, and immunological mediators.

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The Matrix Metalloproteinase Inhibitor Prinomastat Enhances Photodynamic Therapy Responsiveness in a Mouse Tumor Model

Cited by 115 publications

References 23 publications

Intracellular signaling mechanisms in photodynamic therapy

Intracellular signaling mechanisms in photodynamic therapy

Possible in vivo mechanisms involved in photodynamic therapy using tetrapyrrolic macrocycles

Effect of photodynamic therapy on the extracellular matrix and associated components

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