Genetic Aberrations Associated with Photodynamic Therapy in Colorectal Cancer Cells
Identifieur interne : 000801 ( Main/Merge ); précédent : 000800; suivant : 000802Genetic Aberrations Associated with Photodynamic Therapy in Colorectal Cancer Cells
Auteurs : Heidi Abrahamse ; Nicolette Nadene HoureldSource :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
Photodynamic therapy (PDT) is a cancer treatment modality that utilizes three components: light (λ 650–750 nm), a photosensitizer (PS) and molecular oxygen, which upon activation renders the modality effective. Colorectal cancer has one of the highest incident rates as well as a high mortality rate worldwide. In this study, a zinc (Zn) metal-based phthalocyanine (ZnPcSmix) PS was used to determine its efficacy for the treatment of colon adenocarcinoma cells (DLD-1 and Caco-2). Photoactivation of the PS was achieved by laser irradiation at a wavelength of 680 nm. Dose responses were performed to establish optimal PS concentration and irradiation fluence. A working combination of 20 µM ZnPcSmix and 5 J/cm2 was used. Biochemical responses were determined after 1 or 24 h incubation post-treatment. Since ZnPcSmix is localized in lysosomes and mitochondria, mitochondrial destabilization analysis was performed monitoring mitochondrial membrane potential (MMP). Cytosolic acidification was determined measuring hydrogen peroxide (H2O2) levels in the cytoplasm. Having established apoptotic cell death induction, an apoptosis PCR array was performed to establish the apoptotic mechanism. In DLD-1 cells, expression of genes included 3 up-regulated and 20 down-regulated genes while in Caco-2 cells, there were 16 up-regulated and 22 down-regulated genes. In both cell lines, in up-regulated genes, there was a combination of pro- and anti-apoptotic genes that were significantly expressed. Gene expression results showed that more tumorigenic cells (DLD-1) went through apoptosis; however, they exhibit increased risk of resistance and recurrence, while less tumorigenic Caco-2 cells responded better to PDT, thus being suggestive of a better prognosis post-PDT treatment. In addition, the possible apoptotic mechanisms of cell death were deduced based on the genetic expression profiling of regulatory apoptotic inducing factors.
Url:
DOI: 10.3390/ijms20133254
PubMed: 31269724
PubMed Central: 6651415
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Genetic Aberrations Associated with Photodynamic Therapy in Colorectal Cancer Cells</title><author><name sortKey="Abrahamse, Heidi" sort="Abrahamse, Heidi" uniqKey="Abrahamse H" first="Heidi" last="Abrahamse">Heidi Abrahamse</name></author><author><name sortKey="Houreld, Nicolette Nadene" sort="Houreld, Nicolette Nadene" uniqKey="Houreld N" first="Nicolette Nadene" last="Houreld">Nicolette Nadene Houreld</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31269724</idno><idno type="pmc">6651415</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6651415</idno><idno type="RBID">PMC:6651415</idno><idno type="doi">10.3390/ijms20133254</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000605</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000605</idno><idno type="wicri:Area/Pmc/Curation">000605</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000605</idno><idno type="wicri:Area/Pmc/Checkpoint">000742</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000742</idno><idno type="wicri:Area/Ncbi/Merge">000765</idno><idno type="wicri:Area/Ncbi/Curation">000765</idno><idno type="wicri:Area/Ncbi/Checkpoint">000765</idno><idno type="wicri:Area/Main/Merge">000801</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Genetic Aberrations Associated with Photodynamic Therapy in Colorectal Cancer Cells</title><author><name sortKey="Abrahamse, Heidi" sort="Abrahamse, Heidi" uniqKey="Abrahamse H" first="Heidi" last="Abrahamse">Heidi Abrahamse</name></author><author><name sortKey="Houreld, Nicolette Nadene" sort="Houreld, Nicolette Nadene" uniqKey="Houreld N" first="Nicolette Nadene" last="Houreld">Nicolette Nadene Houreld</name></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Photodynamic therapy (PDT) is a cancer treatment modality that utilizes three components: light (λ 650–750 nm), a photosensitizer (PS) and molecular oxygen, which upon activation renders the modality effective. Colorectal cancer has one of the highest incident rates as well as a high mortality rate worldwide. In this study, a zinc (Zn) metal-based phthalocyanine (ZnPcSmix) PS was used to determine its efficacy for the treatment of colon adenocarcinoma cells (DLD-1 and Caco-2). Photoactivation of the PS was achieved by laser irradiation at a wavelength of 680 nm. Dose responses were performed to establish optimal PS concentration and irradiation fluence. A working combination of 20 µM ZnPcSmix and 5 J/cm<sup>2</sup> was used. Biochemical responses were determined after 1 or 24 h incubation post-treatment. Since ZnPcSmix is localized in lysosomes and mitochondria, mitochondrial destabilization analysis was performed monitoring mitochondrial membrane potential (MMP). Cytosolic acidification was determined measuring hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) levels in the cytoplasm. Having established apoptotic cell death induction, an apoptosis PCR array was performed to establish the apoptotic mechanism. In DLD-1 cells, expression of genes included 3 up-regulated and 20 down-regulated genes while in Caco-2 cells, there were 16 up-regulated and 22 down-regulated genes. In both cell lines, in up-regulated genes, there was a combination of pro- and anti-apoptotic genes that were significantly expressed. Gene expression results showed that more tumorigenic cells (DLD-1) went through apoptosis; however, they exhibit increased risk of resistance and recurrence, while less tumorigenic Caco-2 cells responded better to PDT, thus being suggestive of a better prognosis post-PDT treatment. In addition, the possible apoptotic mechanisms of cell death were deduced based on the genetic expression profiling of regulatory apoptotic inducing factors.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Brenner, H" uniqKey="Brenner H">H. Brenner</name></author><author><name sortKey="Kloor, M" uniqKey="Kloor M">M. Kloor</name></author><author><name sortKey="Pox, C P" uniqKey="Pox C">C.P. Pox</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rodriguez, M E" uniqKey="Rodriguez M">M.E. Rodriguez</name></author><author><name sortKey="Zhang, P" uniqKey="Zhang P">P. Zhang</name></author><author><name sortKey="Azizuddin, K" uniqKey="Azizuddin K">K. Azizuddin</name></author><author><name sortKey="Santos, G B D" uniqKey="Santos G">G.B.D. Santos</name></author><author><name sortKey="Chiu, S M" uniqKey="Chiu S">S.-M. Chiu</name></author><author><name sortKey="Xue, L Y" uniqKey="Xue L">L.-Y. 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