Molecular characterization of photosensitizer-mediated photodynamic therapy by gene expression profiling

Liu, KH; Wang, Cheng-Ping; Mf, Chang; Yw, Chung; Lou, Pei‐Jen; Lin, Jianhao

doi:10.1177/0960327113485257

Cited by 6 publications

(5 citation statements)

References 19 publications

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“…Nevertheless, in line with the results of this study, Liu et al . observed significant upregulation of various proinflammatory genes, including FOS , FOSB , IL8, and tumor necrosis factor, alpha-induced protein 3 ( TNFAIP3 ) in 5-aminolevulinic acid (5-ALA)-treated human gingival (Ca9-22) cells [ 32 ]. In our study, SK-ChA-1 cells treated with low-power PDT also demonstrated extensive upregulation of FOS , FOSB , IL8 , and TNFAIP3 (log 2 fold-changes of 4.42, 2.13, 6.75, and 2.75, respectively).…”

Section: Discussionmentioning

confidence: 99%

Low-power photodynamic therapy induces survival signaling in perihilar cholangiocarcinoma cells

et al. 2015

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BackgroundPhotodynamic therapy (PDT) of solid cancers comprises the administration of a photosensitizer followed by illumination of the photosensitizer-replete tumor with laser light. This induces a state of local oxidative stress, culminating in the destruction of tumor tissue and microvasculature and induction of an anti-tumor immune response. However, some tumor types, including perihilar cholangiocarcinoma, are relatively refractory to PDT, which may be attributable to the activation of survival pathways in tumor cells following PDT (i.e., activator protein 1 (AP-1)-, nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-κB)-, hypoxia-inducible factor 1-alpha (HIF-1α)-, nuclear factor (erythroid-derived 2)-like 2 (NFE2L2)-, and unfolded protein response-mediated pathways).MethodsTo assess the activation of survival pathways after PDT, human perihilar cholangiocarcinoma (SK-ChA-1) cells were subjected to PDT with zinc phthalocyanine (ZnPC)-encapsulating liposomes. Following 30-minute incubation with liposomes, the cells were either left untreated or treated at low (50 mW) or high (500 mW) laser power (cumulative light dose of 15 J/cm2). Cells were harvested 90 min post-PDT and whole genome expression analysis was performed using Illumina HumanHT-12 v4 expression beadchips. The data were interpreted in the context of the survival pathways. In addition, the safety of ZnPC-encapsulating liposomes was tested both in vitro and in vivo.ResultsPDT-treated SK-ChA-1 cells exhibited activation of the hypoxia-induced stress response via HIF-1α and initiation of the pro-inflammatory response via NF-кB. PDT at low laser power in particular caused extensive survival signaling, as evidenced by the significant upregulation of HIF-1- (P < 0.001) and NF-кB-related (P < 0.001) genes. Low-power PDT was less lethal to SK-ChA-1 cells 90 min post-PDT, confirmed by annexin V/propidium iodide staining. In vitro toxicogenomics and toxicological testing in chicken embryos and mice revealed that the ZnPC-encapsulating liposomes are non-toxic.ConclusionsPDT-treated perihilar cholangiocarcinoma cells exhibit extensive survival signaling that may translate to a suboptimal therapeutic response and possibly tumor recurrence. These findings encourage the development of photosensitizer delivery systems with co-encapsulated inhibitors of survival pathways.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1994-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Low-power photodynamic therapy induces survival signaling in perihilar cholangiocarcinoma cells

et al. 2015

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“…Liu et al identified three different genes (matrix metalloproteinase 10 ( MMP10 ), Ras homolog enriched in brain like 1 ( RHEBL1 ) and LDL receptor ( LDLR )) whose expression increased due to PDT with four different PS that have different subcellular localization. Although the pathways that explain the overexpression of these genes as a result of PDT remain unclear, these may indicate that there are a set of genes that are related to response to PDT [ 244 ]. In the same way, further characterization of mechanisms of cellular uptake and death still lack.…”

Section: Major Challengesmentioning

confidence: 99%

Photodynamic Efficiency: From Molecular Photochemistry to Cell Death

Bacellar

Tsubone

Pavani

et al. 2015

IJMS

326

267

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Photodynamic therapy (PDT) is a clinical modality used to treat cancer and infectious diseases. The main agent is the photosensitizer (PS), which is excited by light and converted to a triplet excited state. This latter species leads to the formation of singlet oxygen and radicals that oxidize biomolecules. The main motivation for this review is to suggest alternatives for achieving high-efficiency PDT protocols, by taking advantage of knowledge on the chemical and biological processes taking place during and after photosensitization. We defend that in order to obtain specific mechanisms of cell death and maximize PDT efficiency, PSes should oxidize specific molecular targets. We consider the role of subcellular localization, how PS photochemistry and photophysics can change according to its nanoenvironment, and how can all these trigger specific cell death mechanisms. We propose that in order to develop PSes that will cause a breakthrough enhancement in the efficiency of PDT, researchers should first consider tissue and intracellular localization, instead of trying to maximize singlet oxygen quantum yields in in vitro tests. In addition to this, we also indicate many open questions and challenges remaining in this field, hoping to encourage future research.

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“…By incubating oral squamous carcinoma Ca9-22 cells with four types of photosensitizers, Liu et al. ( 24 ) compared the genes differentially expressed between CRC cells with or without PDT treatment and found that LDLR, MMP10, and RHEBL1 had significant changes in all photosensitizer-mediated PDTs. As for CRC, Abrahamse et al.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms of the acquisition of PDT resistance are complex, partially due to the numerous changes in genes and pathways that PDT treatment on cancer cells. By incubating oral squamous carcinoma Ca9-22 cells with four types of photosensitizers, Liu et al (24) compared the genes differentially expressed between CRC cells with or without PDT treatment and found that LDLR, MMP10, and RHEBL1 had significant changes in all photosensitizer-mediated PDTs. As for CRC, Abrahamse et al (25) found three upregulated and 20 downregulated genes within DLD-1 cells, while 16 upregulated and 22 downregulated genes within Caco-2 cells following a zinc (Zn) metal-based phthalocyanine (ZnPcSmix)-mediated PDT.…”

Section: Discussionmentioning

confidence: 99%

A Novel Mechanism of the c-Myc/NEAT1 Axis Mediating Colorectal Cancer Cell Response to Photodynamic Therapy Treatment

et al. 2021

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Photodynamic therapy (PDT) is considered a potential treatment regimen for colorectal cancer cases (CRC). p53 signaling and the miR-124/iASPP axis play an essential role in the PDT resistance of CRC cells. PDT treatment downregulated NEAT1 expression in p53wt HCT116 and RKO cells. In these two cell lines, NEAT1 silencing enhanced the suppressive effects of PDT on cell viability and apoptosis. Within the subcutaneously implanted tumor model, NEAT1 silencing enhanced PDT-induced suppression on tumor growth. Regarding p53-deleted HCT116 cells, PDT only moderately affected cell proliferation but induced downregulation of NEAT1. NEAT1 directly targeted miR-124, acting as a ceRNA, competing with iASPP for miR-124 binding, and counteracting miR-124–mediated repression on iASPP under PDT treatment. NEAT1 silencing was enhanced, whereas miR-124 inhibition attenuated PDT effects on CRC cells; miR-124 inhibition significantly reversed the roles of NEAT1 silencing in PDT-treated CRC cells. miR-124 negatively correlated with NEAT1 and iASPP, respectively, whereas NEAT1 and iASPP positively correlated with each other. PDT downregulated c-Myc in CRC cells, and c-Myc activated the transcription of NEAT1 through the targeting of its promoter region. Within p53mut SW480 cells, PDT failed to alter cell viability and apoptosis but still downregulated c-Myc, NEAT1, and iASPP and upregulated miR-124. In p53 mutant high-abundant CRC tissues, c-Myc and NEAT1 were up-regulated, and miR-124 was downregulated. In c-Myc high-abundant CRC tissues, NEAT1 and iASPP were up-regulated, and miR-124 was downregulated. The critical role of the c-Myc/NEAT1 axis in mediating CRC response to PDT treatment via the miR-124/iASPP/p53 feedback loop was conclusively demonstrated.

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Molecular characterization of photosensitizer-mediated photodynamic therapy by gene expression profiling

Cited by 6 publications

References 19 publications

Low-power photodynamic therapy induces survival signaling in perihilar cholangiocarcinoma cells

Low-power photodynamic therapy induces survival signaling in perihilar cholangiocarcinoma cells

Photodynamic Efficiency: From Molecular Photochemistry to Cell Death

A Novel Mechanism of the c-Myc/NEAT1 Axis Mediating Colorectal Cancer Cell Response to Photodynamic Therapy Treatment

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