Nitric oxide-mediated activity in anti-cancer photodynamic therapy

Rapozzi, Valentina; Pietra, Emilia Della; Zorzet, Sonia; Zacchigna, Marina; Bonavida, Benjamin; Xodo, Luigi E.

doi:10.1016/j.niox.2013.01.002

Cited by 78 publications

(61 citation statements)

References 53 publications

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“…Importantly, apoptosis induction by photodynamic therapy was inhibited in their experiments when the activity of NOS was blocked (54,55). Therefore, it is obvious that under the conditions of the test system described by Rapozzi et al, the concentration of singlet oxygen was not sufficiently high to cause direct apoptosis induction.…”

Section: Figure 3 Inactivation Of Catalase By Low Concentrations Of mentioning

confidence: 96%

The Antitumor Effect of Singlet Oxygen

Bauer

2016

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Section: Figure 3 Inactivation Of Catalase By Low Concentrations Of mentioning

confidence: 96%

The Antitumor Effect of Singlet Oxygen

Bauer

2016

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“…112,113 PDT induces iNOS in tumor cells in vivo and also activates inflammatory cells to produce NO. 114 As a result of the above findings and the role of NO in PDT, Rapozzi et al 115 hypothesized that the efficacy of PDT inhibitory activity may be enhanced by the addition of an exogenous NO donor such as DETANONOate. 116 The findings by Rapozzi et al, 115 using the B78-H1 amelanotic melanoma cells both in vitro and in vivo , demonstrated the effectiveness of the treatment with both PDT and DETANONOate.…”

Section: Induciton Of Rkip By Various Agents and Reversal Of Resimentioning

confidence: 99%

“…114 As a result of the above findings and the role of NO in PDT, Rapozzi et al 115 hypothesized that the efficacy of PDT inhibitory activity may be enhanced by the addition of an exogenous NO donor such as DETANONOate. 116 The findings by Rapozzi et al, 115 using the B78-H1 amelanotic melanoma cells both in vitro and in vivo , demonstrated the effectiveness of the treatment with both PDT and DETANONOate. Treatment with the photosensitizer Pba induced iNOS and inhibited the antiapoptotic effects by interfering with the dysregulated NF-κB/Snail/RKIP loop, namely, inhibition of NF-κB and Snail and induction of RKIP.…”

Section: Induciton Of Rkip By Various Agents and Reversal Of Resimentioning

confidence: 99%

RKIP-Mediated Chemo-Immunosensitization of Resistant Cancer Cells via Disruption of the NF-κB/Snail/YY1/RKIP Resistance-Driver Loop

Bonavida

2014

Crit Rev Oncog

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Cancer remains one of the most dreadful diseases. Whereas most treatment regimens for various cancers have resulted in improved clinical responses and sometimes cures, unfortunately, subsets of cancer patients are either pre-treatment resistant or develop resistance following therapy. These subsets of patients develop cross-resistance to unrelated therapeutics and usually succumb to death. Thus, delineating the underlying molecular mechanisms of resistance of various cancers and identifying molecular targets for intervention are the current main focus of research investigations. One approach to investigate cancer resistance has been to identify pathways that regulate resistance and develop means to disrupt these pathways in order to override resistance and sensitize the resistant cells to cell death. Hence, we have identified one pathway that is dysregulated in cancer, namely, the NF-κB/Snail/YY1/RKIP loop, that has been shown to regulate, in large part, tumor cell resistance to apoptosis by chemotherapeutic and immunotherapeutic cytotoxic drugs. The dysregulated resistant loop is manifested by the overexpression of NF-κB, Snail and YY1 activities and the underexpression of RKIP. The induction of RKIP expression results in the downregulation of NF-κB, Snail and YY1 and the sensitization of resistant cells to drug-induced apoptosis. These findings identified RKIP, in addition to its anti-proliferative and metastatic suppressor functions, as an anti-resistance factor. This brief review describes the role of RKIP in the regulation of drug sensitivity via disruption of the NF-κB/Snail/YY1/RKIP loop that regulates resistance in cancer cells.

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“…Subsequently, different laboratories reported the induction of NO from different PS with apparently contrasting results. While some studies demonstrated a protective effect induced by NO [78,79], others reported an increase of apoptosis in tumor cells induced by high levels of NO [80]. There are different molecular pathways modulated by NO that can stimulate or arrest the tumor growth and these particular pathways can also modulate the cell response to PDT.…”

Section: Role Of Nitric Oxide In Pdtmentioning

confidence: 99%

“…Other molecular pathways modulated by NO that able to influence the PDT tumor response are (i) the WAF1/CIP1/p21 pathway [86,87] that, together with an overexpression of p53, can induce the blockade of the cell cycle and activate the apoptotic pathways [77,88]; (ii) the HIF-1 alpha protein, involved in angiogenesis, inflammation and cell proliferation [89,90]; and (iii) the NF-κB/Snail/YY1/RKIP circuitry [58,80,91].…”

Section: Role Of Nitric Oxide In Pdtmentioning

confidence: 99%

Basic and Clinical Aspects of Photodynamic Therapy

Rapozzi

Jori

2014

Resistance to Targeted Anti-Cancer Therapeutics

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Photodynamic therapy (PDT) was originally developed for the treatment of solid tumors by the concerted action of a tumor-localizing agent, named as the photosensitizer, molecular oxygen and visible light source. The photoinduced cytotxic species are mainly represented by singlet oxygen ( 1 O 2 ), even though the formation of NO has been observed in selected situations. Optimal results are generally obtained by using porphyrins and their tetrapyrrolic analogues as the photodynamic agents, since these compounds display an intense absorbance of the red spectra wavelengths, which are endowed with a particularly deep penetration into most biological tissues. While several porphyrins exhibit an intrinsic preferential affinity for malignant tissues, the selectivity of the tumor localization can be significantly enhanced by pre-binding the photosensitizer with a targeting agent, such as an antibody or a vehicle (e.g., glycoproteins, peptides, oligonucleotide aptamers, growth factors, lipoproteins) directed against antigens or receptors which are specifically present at the surface of tumor cells. Recently, novel perspectives have been opened by the association of the photosensitizer with nanoparticles, which can be made to be multifunctional, thereby allowing the simultaneous delivery of photoactivatable moieties acting by different mechanisms, as well as of phototherapeutic and photodiagnostic agents. The chemical structure of the photosensitizer and the nature of the possible carrier have important consequences with regards to the distribution of the photosensitizer among different compartments of the tumor tissue, such as neoplastic cells, blood vessels or the non-vascular stroma, as well as its localization in different subcellular sites; these would obviously affect the mechanism of photoinduced tumor damage, modulating the competition between necrosis, apoptosis and autophagia, the importance of photoinduced hypoxia, and the balance between enhancement of the immune response and immunosuppression. So far, about 250 randomized clinical trials have been officially reported for 4 V. Rapozzi and G. Jori PDT of tumors, and essentially all types of solid tumors with the exception of melanotic melanoma have been found to be positively responsive to the photodynamic treatment. Thus, PDT is currently considered as a reasonable option for the treatment of a variety of malignant lesions for curative or palliative purposes by using either external or endoscopic irradiation approaches via non-coherent or laser light sources.

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Nitric oxide-mediated activity in anti-cancer photodynamic therapy

Cited by 78 publications

References 53 publications

The Antitumor Effect of Singlet Oxygen

The Antitumor Effect of Singlet Oxygen

RKIP-Mediated Chemo-Immunosensitization of Resistant Cancer Cells via Disruption of the NF-κB/Snail/YY1/RKIP Resistance-Driver Loop

Basic and Clinical Aspects of Photodynamic Therapy

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