Combination of Phosphatidylinositol 3‐Kinases Pathway Inhibitor and Photodynamic Therapy in Endothelial and Tumor Cells
Identifieur interne : 001412 ( Main/Exploration ); précédent : 001411; suivant : 001413Combination of Phosphatidylinositol 3‐Kinases Pathway Inhibitor and Photodynamic Therapy in Endothelial and Tumor Cells
Auteurs : Babasola Fateye [États-Unis] ; Weihua Li [États-Unis] ; Chenguang Wang [États-Unis] ; Bin Chen [États-Unis]Source :
- Photochemistry and Photobiology [ 0031-8655 ] ; 2012-09.
English descriptors
- Teeft :
- Absorption values, Anova test, Apoptosis, Assay, Autophagic, Autophagosome, Autophagosome degradation, Autophagosome formation, Autophagy, Babasola fateye, Cancer cells, Cell death, Cell growth, Cell growth inhibition, Cell lines, Cell proliferation, Cell survival, Chloroquine, Combination therapy, Control value, Endothelial, Endothelial cells, Family proteins, Greater inhibition, Higher dose, Inhibitor, Isoform, Kinase, Mtor, Mutation, Parp, Parp cleavage, Pathway, Phosphatidylinositol, Photodynamic, Photodynamic therapy, Pi3k, Pi3k inhibitor, Pi3k mutations, Pi3k pathway, Pi3k pathway inhibitor, Present study, Proliferation, Prostate, Prostate cancer, Prostate cancer cells, Svec, Svec cells, Tumor cells, Tumor vasculature, Vpdt, Western blot analysis.
Abstract
Tumor recurrence due to incomplete eradication of tumor cells is a major problem facing current cancer therapies. To overcome this problem, it is necessary to enhance cell killing and/or prevent cell regrowth after treatment. Because phosphatidylinositol 3‐kinases (PI3K) pathway plays an important role in stimulating cell survival and growth, we studied the feasibility of using a PI3K pathway inhibitor NVP‐BEZ235 (BEZ235) to enhance the effectiveness of vascular‐targeted photodynamic therapy (vPDT) with verteporfin. We found that BEZ235 or PDT alone significantly inhibited cell growth in both SVEC endothelial and PC‐3 prostate cancer cells, although SVEC cells appeared to be more responsive than PC‐3 cells. Autophagy was detected after both BEZ235 and verteporfin‐PDT in both cell lines. Autophagy appeared to protect cells from PDT‐induced cell death because inhibition of autophagy increased cell death. Autophagic flux assay revealed that PDT actually decreased autophagic flux especially at a high dose of verteporfin. Combination of BEZ235 and PDT caused greater inhibition of PI3K signaling pathway, leading to enhanced cell growth inhibition in both cell lines. SVEC cells exhibited a higher sensitivity towards such a combination than PC‐3 cells. Our data indicated that BEZ235 in combination with PDT provides a promising approach of enhancing therapeutic response.
We studied the interaction between a phosphatidylinositol 3‐kinases (PI3K) pathway inhibitor NVP‐BEZ235 (BEZ235) and photodynamic therapy (PDT) with photosensitizer verteporfin in SVEC endothelial and PC‐3 prostate cancer cells. Our results demonstrated that BEZ235 in combination with verteporfin resulted in enhanced cell growth inhibition in both cell lines. The combination therapy induced greater inhibition of PI3K signaling than each individual therapy.
Url:
DOI: 10.1111/j.1751-1097.2012.01160.x
Affiliations:
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last="Fateye">Babasola Fateye</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Pharmaceutical Sciences, Philadelphia College of Pharmacy, University of the Sciences, Philadelphia</wicri:cityArea></affiliation></author><author><name sortKey="Li, Weihua" sort="Li, Weihua" uniqKey="Li W" first="Weihua" last="Li">Weihua Li</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia</wicri:cityArea></affiliation></author><author><name sortKey="Wang, Chenguang" sort="Wang, Chenguang" uniqKey="Wang C" first="Chenguang" last="Wang">Chenguang Wang</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region 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unit="issue">5</biblScope><biblScope unit="page" from="1265">1265</biblScope><biblScope unit="page" to="1272">1272</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2012-09">2012-09</date></imprint><idno type="ISSN">0031-8655</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0031-8655</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Absorption values</term><term>Anova test</term><term>Apoptosis</term><term>Assay</term><term>Autophagic</term><term>Autophagosome</term><term>Autophagosome degradation</term><term>Autophagosome formation</term><term>Autophagy</term><term>Babasola fateye</term><term>Cancer cells</term><term>Cell death</term><term>Cell growth</term><term>Cell growth inhibition</term><term>Cell lines</term><term>Cell proliferation</term><term>Cell survival</term><term>Chloroquine</term><term>Combination therapy</term><term>Control value</term><term>Endothelial</term><term>Endothelial cells</term><term>Family proteins</term><term>Greater inhibition</term><term>Higher dose</term><term>Inhibitor</term><term>Isoform</term><term>Kinase</term><term>Mtor</term><term>Mutation</term><term>Parp</term><term>Parp cleavage</term><term>Pathway</term><term>Phosphatidylinositol</term><term>Photodynamic</term><term>Photodynamic therapy</term><term>Pi3k</term><term>Pi3k inhibitor</term><term>Pi3k mutations</term><term>Pi3k pathway</term><term>Pi3k pathway inhibitor</term><term>Present study</term><term>Proliferation</term><term>Prostate</term><term>Prostate cancer</term><term>Prostate cancer cells</term><term>Svec</term><term>Svec cells</term><term>Tumor cells</term><term>Tumor vasculature</term><term>Vpdt</term><term>Western blot analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tumor recurrence due to incomplete eradication of tumor cells is a major problem facing current cancer therapies. To overcome this problem, it is necessary to enhance cell killing and/or prevent cell regrowth after treatment. Because phosphatidylinositol 3‐kinases (PI3K) pathway plays an important role in stimulating cell survival and growth, we studied the feasibility of using a PI3K pathway inhibitor NVP‐BEZ235 (BEZ235) to enhance the effectiveness of vascular‐targeted photodynamic therapy (vPDT) with verteporfin. We found that BEZ235 or PDT alone significantly inhibited cell growth in both SVEC endothelial and PC‐3 prostate cancer cells, although SVEC cells appeared to be more responsive than PC‐3 cells. Autophagy was detected after both BEZ235 and verteporfin‐PDT in both cell lines. Autophagy appeared to protect cells from PDT‐induced cell death because inhibition of autophagy increased cell death. Autophagic flux assay revealed that PDT actually decreased autophagic flux especially at a high dose of verteporfin. Combination of BEZ235 and PDT caused greater inhibition of PI3K signaling pathway, leading to enhanced cell growth inhibition in both cell lines. SVEC cells exhibited a higher sensitivity towards such a combination than PC‐3 cells. Our data indicated that BEZ235 in combination with PDT provides a promising approach of enhancing therapeutic response.</div><div type="abstract">We studied the interaction between a phosphatidylinositol 3‐kinases (PI3K) pathway inhibitor NVP‐BEZ235 (BEZ235) and photodynamic therapy (PDT) with photosensitizer verteporfin in SVEC endothelial and PC‐3 prostate cancer cells. Our results demonstrated that BEZ235 in combination with verteporfin resulted in enhanced cell growth inhibition in both cell lines. The combination therapy induced greater inhibition of PI3K signaling than each individual therapy.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Fateye, Babasola" sort="Fateye, Babasola" uniqKey="Fateye B" first="Babasola" last="Fateye">Babasola Fateye</name></region><name sortKey="Chen, Bin" sort="Chen, Bin" uniqKey="Chen B" first="Bin" last="Chen">Bin Chen</name><name sortKey="Chen, Bin" sort="Chen, Bin" uniqKey="Chen B" first="Bin" last="Chen">Bin Chen</name><name sortKey="Li, Weihua" sort="Li, Weihua" uniqKey="Li W" first="Weihua" last="Li">Weihua Li</name><name sortKey="Wang, Chenguang" sort="Wang, Chenguang" uniqKey="Wang C" first="Chenguang" last="Wang">Chenguang Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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