In Vitro Induction of PDT Resistance in HT29, HT1376 and SK-N-MC Cells by Various Photosensitizers¶

Singh, Gurmit; Espiritu, Myrna; Shen, Xiao Yun; Hanlon, John G.; Rainbow, Andrew J.

doi:10.1562/0031-8655(2001)0730651iviopr2.0.co2

Cited by 15 publications

(27 citation statements)

References 6 publications

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“…The induction of resistance was achieved by in vitro photodynamic treatments with Photofrin to the 1–10% survival level followed by regrowth of single surviving colonies. (25). In spite of the difference in the uptake of Photofrin between the resistant cells and parental cells, changes in the stress protein expression were observed in the resistant variants (21).…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of heat‐shock protein 27–induced resistance to photodynamic therapy in oral cancer cells

Kim

Jung

Lim

et al. 2012

J Oral Pathology Medicine

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Photodynamic therapy (PDT) of cells is a new treatment modality involving selective delivery of a photosensitive dye into target cells, followed by visible light irradiation. PDT induces cell death by excessive ROS generation. The effects of multiple photosensitizers were owing to the difference in cell types involving sensitizer-specific protein changes linked to resistance. HSP27 is regulated in response to stress and is associated with apoptotic process. The effects of HSP27 on PDT resistance are controversial and unclear. The purpose of this study was to investigate the role of HSP27 down-regulation in the PDT-induced cells and HSP27 regulation in the resistance to PDT. KB cells transfected with HSP27 siRNA were exposed to hematoporphyrin (HP) followed by irradiation at 635 nm at an energy density of 4.5 mW/cm(2). After irradiation, the effects on HSP27 down-regulation were assessed by MTT assay, flow cytometry, confocal analysis, Western blotting and caspase activity. The results of this study showed that down-regulation of HSP27 restored cell survival in HP-PDT-induced apoptotic KB cells. HSP27 down-regulation attenuated PDT-induced apoptosis through caspase-mediated pathway in KB cells. Also, HSP27 silencing regulated Bax, Bcl-2, and PARP protein expression in PDT-induced cells. Therefore, HSP27 down-regulation confers resistance to PDT through interruption of apoptotic protein activity in PDT-induced cell death. HSP27 might contribute to regulating PDT-induced apoptosis in PDT-resistant cells.

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Section: Discussionmentioning

confidence: 99%

Down‐regulation of heat‐shock protein 27–induced resistance to photodynamic therapy in oral cancer cells

Kim

Jung

Lim

et al. 2012

J Oral Pathology Medicine

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“…The protocol of in vitro induction was modified from the standard protocol as described in previous reports [30,31]. The light source for selection of PDT-resistant cells was a semiconductor diode laser (Diomed 630 MED from Diomed, Inc.).…”

Section: Selection Of Pdt-resistant Esophageal Squamous Carcinoma Cellsmentioning

confidence: 99%

The effect of ephrin-A1 on resistance to Photofrin-mediated photodynamic therapy in esophageal squamous cell carcinoma cells

et al. 2015

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Esophageal squamous cell carcinoma (ESCC), the most prevalent cell type of esophageal cancer, remains a dismal disease with poor prognosis. Photodynamic therapy (PDT) is a minimally invasive treatment option for early esophageal cancer. To explore possible factors involved in resistance to PDT in esophageal cancer cells, we selected PDT-resistant subcell lines by repeated treatment of CE48T/VGH (CE48T) ESCC cells with Photofrin-PDT and then analyzed the global gene modulations in the PDT-resistant cells by whole-genome microarray. More than 700 genes reached a fold change greater than 1.5 in each of the PDT-resistant cells compared to parental cells. Among these genes, both tumor necrosis factor (TNF) and EFNA1 genes were significantly upregulated in resistant cell lines. However, they were significantly downregulated in Photofrin-PDT-treated cells compared to untreated cells. The observations made in the microarray analysis were further confirmed by quantitative PCR. We observed that recombinant tumor necrosis factor alpha (TNF-α) activated the gene expression of EFNA1 at both the messenger RNA (mRNA) level and the protein level in CE48T cells. Functional analysis showed that when incubated with oligomeric and monomeric ephrin-A1 simultaneously, ESCC cells became significantly resistant to Photofrin-PDT. Functional analysis further suggested that transmembrane and soluble ephrin-A1 may cooperate to enhance resistance to Photofrin-PDT in ESCC cells.

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“…The ratios of increased survival at the LD90 level ranged between 1.5-and ca. 3-fold more resistant[72].Kulbacka et al studied phototoxic effect of Photofrin® against doxorubicin sensitive (LoVo) and resistant (LoVoDX) CRC cell lines. Photosensitizer of concentration 15 and 30 mg/l was administered to cell culture.…”

mentioning

confidence: 99%

Photodynamic therapy in colorectal cancer treatment—The state of the art in preclinical research

Kawczyk‐Krupka

Bugaj

Latos

et al. 2016

Photodiagnosis and Photodynamic Therapy

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In Vitro Induction of PDT Resistance in HT29, HT1376 and SK-N-MC Cells by Various Photosensitizers¶

Cited by 15 publications

References 6 publications

Down‐regulation of heat‐shock protein 27–induced resistance to photodynamic therapy in oral cancer cells

Down‐regulation of heat‐shock protein 27–induced resistance to photodynamic therapy in oral cancer cells

The effect of ephrin-A1 on resistance to Photofrin-mediated photodynamic therapy in esophageal squamous cell carcinoma cells

Photodynamic therapy in colorectal cancer treatment—The state of the art in preclinical research

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