Rose Bengal Acetate photodynamic therapy-induced autophagy

Dini, Luciana; Inguscio, Valentina; Tenuzzo, Bernardetta Anna; Panzarini, Elisa

doi:10.4161/cbt.10.10.13371

Cited by 26 publications

(23 citation statements)

References 39 publications

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“…In particular, mitochondrial- and ER-localized PSs trigger a pro-survival autophagic response to recycle injured organelles [132,133], while, PSs localized and damaging lysosomes block autophagosome formation, thus leading to autophagy inhibition. It has been further demonstrated that also PSs localizing in mitochondria or ER after relocation from their primary damage site, induce autophagic cell death [134,135] in addition to apoptosis [136,137]. The kinetic of apoptosis/autophagy switch strictly depends on cell type, PS type and concentration and light dose.…”

Section: Autophagy-assisted Cancer Therapy: Old and New Insightsmentioning

confidence: 99%

Nanomaterials and Autophagy: New Insights in Cancer Treatment

Panzarini

Inguscio

Tenuzzo

et al. 2013

Cancers

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Autophagy represents a cell’s response to stress. It is an evolutionarily conserved process with diversified roles. Indeed, it controls intracellular homeostasis by degradation and/or recycling intracellular metabolic material, supplies energy, provides nutrients, eliminates cytotoxic materials and damaged proteins and organelles. Moreover, autophagy is involved in several diseases. Recent evidences support a relationship between several classes of nanomaterials and autophagy perturbation, both induction and blockade, in many biological models. In fact, the autophagic mechanism represents a common cellular response to nanomaterials. On the other hand, the dynamic nature of autophagy in cancer biology is an intriguing approach for cancer therapeutics, since during tumour development and therapy, autophagy has been reported to trigger both an early cell survival and a late cell death. The use of nanomaterials in cancer treatment to deliver chemotherapeutic drugs and target tumours is well known. Recently, autophagy modulation mediated by nanomaterials has become an appealing notion in nanomedicine therapeutics, since it can be exploited as adjuvant in chemotherapy or in the development of cancer vaccines or as a potential anti-cancer agent. Herein, we summarize the effects of nanomaterials on autophagic processes in cancer, also considering the therapeutic outcome of synergism between nanomaterials and autophagy to improve existing cancer therapies.

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Section: Autophagy-assisted Cancer Therapy: Old and New Insightsmentioning

confidence: 99%

Nanomaterials and Autophagy: New Insights in Cancer Treatment

Panzarini

Inguscio

Tenuzzo

et al. 2013

Cancers

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“…Noteworthy, in Dini’s laboratory it is demonstrated that Rose Bengale Acetate, a PS localizing in ER only after redistribution from its perinuclear primary damage site induces autophagic cell death [107,108] in addition to apoptosis [109,110] in human epitheloid cervix carcinoma HeLa cells. …”

Section: Autophagy In Pdt-photosensitized Cellsmentioning

confidence: 99%

Autophagy Contributes to the Death/Survival Balance in Cancer PhotoDynamic Therapy

Inguscio

Panzarini

Dini

2012

Cells

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Autophagy is an important cellular program with a “double face” role, since it promotes either cell survival or cell death, also in cancer therapies. Its survival role occurs by recycling cell components during starvation or removing stressed organelles; when damage becomes extensive, autophagy provides another programmed cell death pathway, known as Autophagic Cell Death (ACD). The induction of autophagy is a common outcome in PhotoDynamic Therapy (PDT), a two-step process involving the irradiation of photosensitizer (PS)-loaded cancer cells. Upon tissue oxygen interaction, PS provokes immediate and direct Reactive Oxygen Species (ROS)-induced damage to Endoplasmic Reticulum (ER), mitochondria, plasma membrane, and/or lysosomes. The main biological effects carried out in cancer PDT are direct cytotoxicity to tumor cells, vasculature damage and induction of inflammatory reactions stimulating immunological responses. The question about the role of autophagy in PDT and its putative immunological impact is hotly controversial and largely studied in recent times. This review deals with the induction of autophagy in PDT protocols and its dual role, also considering its interrelationship with apoptosis, the preferential cell death program triggered in the photodynamic process.

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“…Here, we evaluate if oxidative stress elicited by Rose Bengal Acetate-PDT (RBAc-PDT) induces in HeLa cells the in vitro biochemical distinctive properties of ICD such as relocalization, i.e., exposure and/or release, of DAMPs in order to make a prediction about the capacity of RBAc to trigger ICD. In fact, in our previous papers we have demonstrated that RBAc-PDT ensures in HeLa cells the rapid, independent and long-lasting onset of apoptosis and autophagy by several signalling pathways originating from or converging on almost all intracellular organelles (mitochondria, lysosomes, Golgi apparatus and ER), despite RBAc primary perinuclear localization [29]–[33]. In addition, we showed that 1) apoptotic and autophagic RBAc photokilled HeLa cells efficiently recruit macrophages; 2) macrophages efficiently phagocyte dead HeLa cells; and 3) macrophages following internalization release IL-10, TGF-β and TNF-α [34].…”

Section: Introductionmentioning

confidence: 99%

Rose Bengal Acetate PhotoDynamic Therapy (RBAc-PDT) Induces Exposure and Release of Damage-Associated Molecular Patterns (DAMPs) in Human HeLa Cells

et al. 2014

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The new concept of Immunogenic Cell Death (ICD), associated with Damage Associated Molecular Patterns (DAMPs) exposure and/or release, is recently becoming very appealing in cancer treatment. In this context, PhotoDynamic Therapy (PDT) can give rise to ICD and to immune response upon dead cells removal. The list of PhotoSensitizers (PSs) able to induce ICD is still short and includes Photofrin, Hypericin, Foscan and 5-ALA. The goal of the present work was to investigate if Rose Bengal Acetate (RBAc), a powerful PS able to trigger apoptosis and autophagy, enables photosensitized HeLa cells to expose and/or release pivotal DAMPs, i.e. ATP, HSP70, HSP90, HMGB1, and calreticulin (CRT), that characterize ICD. We found that apoptotic HeLa cells after RBAc-PDT exposed and released, early after the treatment, high amount of ATP, HSP70, HSP90 and CRT; the latter was distributed on the cell surface as uneven patches and co-exposed with ERp57. Conversely, autophagic HeLa cells after RBAc-PDT exposed and released HSP70, HSP90 but not CRT and ATP. Exposure and release of HSP70 and HSP90 were always higher on apoptotic than on autophagic cells. HMGB1 was released concomitantly to secondary necrosis (24 h after RBAc-PDT). Phagocytosis assay suggests that CRT is involved in removal of RBAc-PDT generated apoptotic HeLa cells. Altogether, our data suggest that RBAc has all the prerequisites (i.e. exposure and/or release of ATP, CRT, HSP70 and HSP90), that must be verified in future vaccination experiments, to be considered a good PS candidate to ignite ICD. We also showed tha CRT is involved in the clearance of RBAc photokilled HeLa cells. Interestingly, RBAc-PDT is the first cancer PDT protocol able to induce the translocation of HSP90 and plasma membrane co-exposure of CRT with ERp57.

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Rose Bengal Acetate photodynamic therapy-induced autophagy

Cited by 26 publications

References 39 publications

Nanomaterials and Autophagy: New Insights in Cancer Treatment

Nanomaterials and Autophagy: New Insights in Cancer Treatment

Autophagy Contributes to the Death/Survival Balance in Cancer PhotoDynamic Therapy

Rose Bengal Acetate PhotoDynamic Therapy (RBAc-PDT) Induces Exposure and Release of Damage-Associated Molecular Patterns (DAMPs) in Human HeLa Cells

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