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Histone deacetylase inhibitors potentiate photochemotherapy in cutaneous T-cell lymphoma MyLa cells

Paper ID Volume ID Publish Year Pages File Format Full-Text
29439 44397 2014 9 PDF Available
Title
Histone deacetylase inhibitors potentiate photochemotherapy in cutaneous T-cell lymphoma MyLa cells
Abstract

•UVASens induces synergistic cell-death and DNA double-strand breaks following activation by UV-A.•The broad-spectrum HDACi, SAHA significantly augments UVASens/UV-A induced cell-death and DNA damage in MyLa cells.•The classI specific HDACi, MS-275 significantly augments UVASens/UV-A induced cell-death and DNA damage in MyLa cells.•UVASens/UV-A phototherapy inhibits the repair kinetics of MyLa cells.

Cutaneous T cell lymphomas (CTCL) represent rare extranodal non-Hodgkin’s lymphomas, which are characterised by pleomorphic skin lesions and distinct T-cell markers. CTCL is a relatively benign disease in its early stages, but survival rates decrease significantly with progression. Histone deacetylase inhibitors (HDACi) have recently emerged as a new class of targeted anticancer therapies for CTCL, which have been shown to induce growth inhibition, terminal differentiation and apoptosis in various cancers in vitro and in vivo. In addition to the intrinsic anticancer properties of HDACi, recent studies have demonstrated its ability to synergise with phototherapy. In particular, we examine the therapeutic potential of HDACi in combination with ultraviolet A (UV-A) phototherapy, employing a halogenated DNA minor groove binding ligand called UVASens as a photosensitiser. In vitro studies have demonstrated that UVASens is approximately 1000-fold more potent than current psoralens. The extreme photopotency of UVASens allows the use of lower radiation doses minimising the carcinogenic risks associated with the long-term use of phototherapy. Considering, previous findings using the photosensitiser UVASens and potential synergy of HDACi with phototherapy, it was hypothesised that HDACi will augment photochemotherapy-induced cytotoxicity in CTCL MyLa cells. The findings indicated that combinations of UVASens/UV-A photochemotherapy and HDACi significantly decreased cell viability and increased apoptosis and DNA double-strand breaks in MyLa cells.

Keywords
Phototherapy; Iodinated DNA ligand; Histone deacetylases; Histone deacetylase inhibitors; Cutaneous T-cell lymphoma; DNA double-strand breaks
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Histone deacetylase inhibitors potentiate photochemotherapy in cutaneous T-cell lymphoma MyLa cells
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Publisher
Database: Elsevier - ScienceDirect
Journal: Journal of Photochemistry and Photobiology B: Biology - Volume 131, 5 February 2014, Pages 104–112
Authors
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Subjects
Physical Sciences and Engineering Chemical Engineering Bioengineering
Get Full-Text Now
Don't Miss Today's Special Offer
Price was $35.95
You save - $31
Price after discount Only $4.95
100% Money Back Guarantee
Full-text PDF Download
Online Support
Any Questions? feel free to contact us