In vitro and in vivo matrix metalloproteinase expression after photodynamic therapy with a liposomal formulation of aminolevulinic acid and its methyl ester

Osiecka, Beata J.; Jurczyszyn, Kamil; Symonowicz, Krzysztof; Bronowicz, Andrzej; Ostasiewicz, Paweł; Czapińska, Elżbieta; Hotowy, Katarzyna; Krzystek−Korpacka, Małgorzata; Gębarowska, Elżbieta; Iżykowska, Ilona; Dzięgiel, Piotr; Terlecki, Grzegorz; Ziółkowski, Piotr

doi:10.2478/s11658-010-0033-1

Cited by 14 publications

(5 citation statements)

References 42 publications

(50 reference statements)

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“…Therefore, preliminary data suggest that using MMP inhibitors may potentially enhance clinical PDT. 9 (Although prinomastat was in clinical trials, Dr. Gomer indicates that it is not being studied further at this time. )…”

Section: Discussionmentioning

confidence: 99%

Induction of Prosurvival Molecules During Treatment: Rethinking Therapy Options for Photodynamic Therapy

Gomer¹

2012

J Natl Compr Canc Netw

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Photodynamic therapy (PDT) not only causes direct cytotoxicity to malignant cells within a tumor but also appears to have both direct and indirect effects on nonmalignant components of the tumor microenvironment. A host of preclinical studies have been performed to document how PDT modulates the tumor microenvironment. This article explores the role of cellular components such as the hypoxia-inducible factor 1α, vascular endothelial growth factor, cyclooxygenase-2, matrix metalloproteinases, the antiapoptotic protein survivin, and 17-AAG (an inhibitor of heat shock proteins), with the hope that combined modality regimens targeting these processes may improve PDT tumor responsiveness.

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Section: Discussionmentioning

confidence: 99%

Induction of Prosurvival Molecules During Treatment: Rethinking Therapy Options for Photodynamic Therapy

Gomer¹

2012

J Natl Compr Canc Netw

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“…However, the regulation of MMPs following PDT is ambivalent. For example, MMPs 1–3 were upregulated or activated in HK-1 nasopharyngeal carcinoma cells, MCF-7 mammary carcinoma cells and xenografts, in a Walker carcinosarcoma model, and in keratinocyte-associated fibroblasts that were subjected to PDT [ 240 , 264 – 266 ]. Furthermore, long-term upregulation of MMP9 but not MMP1, MMP3, MMP7, and MMP12 was observed in actinic keratosis patients treated by PDT [ 267 ].…”

Section: Survival Pathways Activated In Tumor Cells Post-pdtmentioning

confidence: 99%

Tumor cell survival pathways activated by photodynamic therapy: a molecular basis for pharmacological inhibition strategies

Broekgaarden

Weijer

Gulik

et al. 2015

Cancer Metastasis Rev

200

156

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Photodynamic therapy (PDT) has emerged as a promising alternative to conventional cancer therapies such as surgery, chemotherapy, and radiotherapy. PDT comprises the administration of a photosensitizer, its accumulation in tumor tissue, and subsequent irradiation of the photosensitizer-loaded tumor, leading to the localized photoproduction of reactive oxygen species (ROS). The resulting oxidative damage ultimately culminates in tumor cell death, vascular shutdown, induction of an antitumor immune response, and the consequent destruction of the tumor. However, the ROS produced by PDT also triggers a stress response that, as part of a cell survival mechanism, helps cancer cells to cope with the PDT-induced oxidative stress and cell damage. These survival pathways are mediated by the transcription factors activator protein 1 (AP-1), nuclear factor E2-related factor 2 (NRF2), hypoxia-inducible factor 1 (HIF-1), nuclear factor κB (NF-κB), and those that mediate the proteotoxic stress response. The survival pathways are believed to render some types of cancer recalcitrant to PDT and alter the tumor microenvironment in favor of tumor survival. In this review, the molecular mechanisms are elucidated that occur post-PDT to mediate cancer cell survival, on the basis of which pharmacological interventions are proposed. Specifically, pharmaceutical inhibitors of the molecular regulators of each survival pathway are addressed. The ultimate aim is to facilitate the development of adjuvant intervention strategies to improve PDT efficacy in recalcitrant solid tumors.

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“…Both MMP‐9 and ‐2 activities were diminished in most of our PDT‐treated populations, which might be quite relevant for invasion and metastasis. Expression of tumor matrix metalloproteinases has been shown to be either increased [Osiecka et al, ] or decreased by PDT treatment with several PSs [Etminan et al, ] either in tumors or in skin wound healing models.…”

Section: Discussionmentioning

confidence: 99%

Reversal of the Migratory and Invasive Phenotype of Ras-Transfected Mammary Cells by Photodynamic Therapy Treatment

et al. 2016

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Photodynamic therapy (PDT) is a non-thermal technique for inducing tumor damage following administration of a light-activated photosensitizing drug (PS). In a previous work we found that PDT induces cytoskeleton changes in HB4a-Ras cells (human mammary breast carcinoma HB4a cells transfected with the RAS oncogene). In the present work we have studied the migratory and invasive features and the expression of proteins related to these processes on HB4a-Ras cells after three successive cycles of PDT using different PSs: 5-aminolevulinic acid (ALA), Verteporfin (Verte), m-tetrahydroxyphenylchlorin (m-THPC), and Merocyanine 540 (MC). A slight (1.25- to 2-fold) degree of resistance was acquired in cell populations subjected to the three successive PDT treatments. However, complete cell killing was achieved after a light dose increase. Regardless of the PS employed, all the PDT-treated populations had shorter stress fibres than the untreated control HB4a-Ras cells, and the number of dorsal stress fibres was decreased in the PDT-treated populations. E-Cadherin distribution, which was already aberrant in HB4a-Ras cells, became even more diffuse in the PDT-treated populations, though its expression was increased in some of them. The strong migratory and invasive ability of HB4a-Ras cells in vitro was impaired in all the PDT-treated populations, with a behavior that was similar to the parental non-tumoral HB4a cells. MMP-2 and -9 metalloproteinase activities were also impaired in the PDT-treated populations. The evidence presented herein suggests that the cells surviving PDT would be less metastatic than the initial population. These findings encourage the use of PDT in combination with other treatments such as intraoperative or post-surgery therapeutic procedures. J. Cell. Biochem. 118: 464-477, 2017. © 2016 Wiley Periodicals, Inc.

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In vitro and in vivo matrix metalloproteinase expression after photodynamic therapy with a liposomal formulation of aminolevulinic acid and its methyl ester

Cited by 14 publications

References 42 publications

Induction of Prosurvival Molecules During Treatment: Rethinking Therapy Options for Photodynamic Therapy

Induction of Prosurvival Molecules During Treatment: Rethinking Therapy Options for Photodynamic Therapy

Tumor cell survival pathways activated by photodynamic therapy: a molecular basis for pharmacological inhibition strategies

Reversal of the Migratory and Invasive Phenotype of Ras-Transfected Mammary Cells by Photodynamic Therapy Treatment

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