2009Xiandai shengwu yixue jinzhanRequires access

Radiosensitizing effect of trichostatin A (TSA) on non-small cell lung cancer A549 cells

Feng Zhang

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Abstract

Objective: To define the activity of trichostatin A (TSA), one of the HDIs, to radiosensitize human non-small cell lung cancer (NSCLC) cell line A549 cells in vitro. Methods: A549 cells were exposed to γ-irradiation with or without TSA co-treatment. MTT assay was performed to evaluate cell viability. Apoptosis was analyzed with Annexin V-PI staining by flow cytometry. Active form of caspase-3 positive cells was measured by flow cytometry. Results: The results showed that co-treatment of TSA 1μM significantly radiosensitized A549 cells to γ-irradiation (5Gy) by decreasing cell viability. γ-irradiation or TSA alone caused only a small amount of apoptotic cells, as indicated by Annexin V positive cells. However, TSA co-treatment significantly enhanced γ-irradiation-induced apoptosis. Meanwhile, in TSA and γ-irradiation co-treatment group, cells positive for caspase-3 active form were significantly increased compared to group treated with γ-irradiation (5Gy) or TSA alone. Conclusions: Taken together, these results suggest that TSA has potential to act as radio-sensitizer in A549 cells by promoting caspase-3 activity and increasing apoptosis.

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Objective: To define the activity of trichostatin A (TSA), one of the HDIs, to radiosensitize human non-small cell lung cancer (NSCLC) cell line A549 cells in vitro. Methods: A549 cells were exposed to γ-irradiation with or without TSA co-treatment. MTT assay was performed to evaluate cell viability. Apoptosis was analyzed with Annexin V-PI staining by flow cytometry. Active form of caspase-3 positive cells was measured by flow cytometry. Results: The results showed that co-treatment of TSA 1μM significantly radiosensitized A549 cells to γ-irradiation (5Gy) by decreasing cell viability. γ-irradiation or TSA alone caused only a small amount of apoptotic cells, as indicated by Annexin V positive cells. However, TSA co-treatment significantly enhanced γ-irradiation-induced apoptosis. Meanwhile, in TSA and γ-irradiation co-treatment group, cells positive for caspase-3 active form were significantly increased compared to group treated with γ-irradiation (5Gy) or TSA alone. Conclusions: Taken together, these results suggest that TSA has potential to act as radio-sensitizer in A549 cells by promoting caspase-3 activity and increasing apoptosis.

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Available abstract

Objective: To define the activity of trichostatin A (TSA), one of the HDIs, to radiosensitize human non-small cell lung cancer (NSCLC) cell line A549 cells in vitro. Methods: A549 cells were exposed to γ-irradiation with or without TSA co-treatment. MTT assay was performed to evaluate cell viability. Apoptosis was analyzed with Annexin V-PI staining by flow cytometry. Active form of caspase-3 positive cells was measured by flow cytometry. Results: The results showed that co-treatment of TSA 1μM significantly radiosensitized A549 cells to γ-irradiation (5Gy) by decreasing cell viability. γ-irradiation or TSA alone caused only a small amount of apoptotic cells, as indicated by Annexin V positive cells. However, TSA co-treatment significantly enhanced γ-irradiation-induced apoptosis. Meanwhile, in TSA and γ-irradiation co-treatment group, cells positive for caspase-3 active form were significantly increased compared to group treated with γ-irradiation (5Gy) or TSA alone. Conclusions: Taken together, these results suggest that TSA has potential to act as radio-sensitizer in A549 cells by promoting caspase-3 activity and increasing apoptosis.

Key concepts: Trichostatin A, A549 cell, Apoptosis, Viability assay, Flow cytometry, Annexin, Chemistry, Molecular biology

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