Photodynamic therapy decreases cancer colonic cell adhesiveness and metastatic potential

Vonarx, Véronique; Foultier, Marie-Thérèse; Brito, Léonor Xavier de; Anasagasti, L.; Morlet, Laurent; Patrice, Thierry

doi:10.1007/bf02576780

Cited by 24 publications

(16 citation statements)

References 36 publications

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“…BPD-MA PDT of fibroblast interfered with cell adhesion without altering integrin expression (Margaron et al, 1997), which is consistent with observations in our study. HPD PDT caused a reduced adhesion of colonic cancer cells to endothelial cells (Vonarx et al, 1995). Other membrane and non-membrane agents also modulate the expression of integrins (Danilov and Juliano, 1989;Conforti et al, 1990;Elices et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

BPD-MA-mediated photosensitization in vitro and in vivo: cellular adhesion and β1 integrin expression in ovarian cancer cells

et al. 1999

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Summary Benzoporphyrin derivative monoacid (BPD-MA) photosensitization was examined for its effects on cellular adhesion of a human ovarian cancer cell line, OVCAR 3, to extracellular matrix (ECM) components. Mild BPD-MA photosensitization (~ 85% cell survival) of OVCAR 3 transiently decreased adhesion to collagen IV, fibronectin, laminin and vitronectin to a greater extent than could be attributed to cell death. The loss in adhesiveness was accompanied by a loss of β 1 integrin-containing focal adhesion plaques (FAPs), although β 1 subunits were still recognized by monoclonal antibody directed against human β 1 subunits. In vivo BPD-MA photosensitization decreased OVCAR 3 adhesiveness as well. Photosensitized adhesion was reduced in the presence of sodium azide and enhanced in deuterium oxide, suggesting mediation by singlet oxygen. Co-localization studies of BPD-MA and Rhodamine 123 showed that the photosensitizer was largely mitochondrial, but also exhibited extramitochondrial, intracellullar, diffuse cytosolic fluorescence. Taken together, these data show that intracellular damage mediated by BPD-PDT remote from the FAP site can affect cellular-ECM interactions and result in loss of FAP formation. This may have an impact on long-term effects of photodynamic therapy. The topic merits further investigation.

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Section: Discussionmentioning

confidence: 99%

BPD-MA-mediated photosensitization in vitro and in vivo: cellular adhesion and β1 integrin expression in ovarian cancer cells

et al. 1999

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“…Following in vitro PDT, adhesiveness of malignant cells to EC, as well as their capability to invade the basement membrane (13) decline. Similarly, Vonarx et al (14) observed that PDT using a hematoporphyrin derivative decreased the adhesiveness of colonic cancer cells to EC monolayers. The effect of PDT was also studied on cadherins, another class of adhesion molecules primarily responsible for the formation of stable junctions between cells in tissues.…”

Section: Adhesion Moleculesmentioning

confidence: 87%

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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“…It has been described an effect of PDT on either decreasing or increasing adhesion to plastic, ECM and to endothelial cells [186, 190, 191]. PDT using BPD-MA inhibited cell adhesion, with no significant differences between matrices and without altering integrin expression [185].…”

Section: Morphology Cell Adhesion Cytoskeleton and Metastasesmentioning

confidence: 99%

“…Three major eukaryotic cytoskeletal proteins are actin, tubulin and intermediate filaments. Any disturbances in these systems have been related to tumor progression and metastasis [191]. Changes in the cell shape (cell attachment, cytoskeleton) in the course of apoptosis execution promote the formation of apoptotic bodies.…”

Section: Morphology Cell Adhesion Cytoskeleton and Metastasesmentioning

confidence: 99%

Mechanisms of Resistance to Photodynamic Therapy

Casas¹,

Venosa²,

Hasan³

et al. 2011

CMC

281

215

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Photodynamic therapy (PDT) involves the administration of a photosensitizer (PS) followed by illumination with visible light, leading to generation of reactive oxygen species. The mechanisms of resistance to PDT ascribed to the PS may be shared with the general mechanisms of drug resistance, and are related to altered drug uptake and efflux rates or altered intracellular trafficking. As a second step, an increased inactivation of oxygen reactive species is also associated to PDT resistance via antioxidant detoxifying enzymes and activation of heat shock proteins. Induction of stress response genes also occurs after PDT, resulting in modulation of proliferation, cell detachment and inducing survival pathways among other multiple extracellular signalling events. In addition, an increased repair of induced damage to proteins, membranes and occasionally to DNA may happen. PDT-induced tissue hypoxia as a result of vascular damage and photochemical oxygen consumption may also contribute to the appearance of resistant cells. The structure of the PS is believed to be a key point in the development of resistance, being probably related to its particular subcellular localization. Although most of the features have already been described for chemoresistance, in many cases, no cross-resistance between PDT and chemotherapy has been reported. These findings are in line with the enhancement of PDT efficacy by combination with chemotherapy. The study of cross resistance in cells with developed resistance against a particular PS challenged against other PS is also highly complex and comprises different mechanisms. In this review we will classify the different features observed in PDT resistance, leading to a comparison with the mechanisms most commonly found in chemo resistant cells.

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Photodynamic therapy decreases cancer colonic cell adhesiveness and metastatic potential

Cited by 24 publications

References 36 publications

BPD-MA-mediated photosensitization in vitro and in vivo: cellular adhesion and β1 integrin expression in ovarian cancer cells

BPD-MA-mediated photosensitization in vitro and in vivo: cellular adhesion and β1 integrin expression in ovarian cancer cells

Effect of photodynamic therapy on the extracellular matrix and associated components

Mechanisms of Resistance to Photodynamic Therapy

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