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Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C

INTRODUCTION: Docosahexaenoic acid (DHA) supplementation has been reported to negatively correlate with cancer cell proliferation and tumour development in many cancer types. Although cumulative evidence has demonstrated the apoptotic effect and cytotoxicity of DHA against tumour development in many...

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Autores principales: Chung, Soo-Ho, Lee, Hae-Hyeog, Kim, Yeon-Suk, Song, Kisung, Kim, Tae-Hee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10074323/
https://www.ncbi.nlm.nih.gov/pubmed/37034541
http://dx.doi.org/10.5114/aoms/111947
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author Chung, Soo-Ho
Lee, Hae-Hyeog
Kim, Yeon-Suk
Song, Kisung
Kim, Tae-Hee
author_facet Chung, Soo-Ho
Lee, Hae-Hyeog
Kim, Yeon-Suk
Song, Kisung
Kim, Tae-Hee
author_sort Chung, Soo-Ho
collection PubMed
description INTRODUCTION: Docosahexaenoic acid (DHA) supplementation has been reported to negatively correlate with cancer cell proliferation and tumour development in many cancer types. Although cumulative evidence has demonstrated the apoptotic effect and cytotoxicity of DHA against tumour development in many cell types, the precise cellular and biochemical mechanisms of DHA-induced apoptosis in human endometrial cancer cells have not been investigated. MATERIAL AND METHODS: MTT assay was performed to confirm the degree of apoptosis by combining treatment with DHA and triacsin C in endometrial cancer cell line. The synergistic effects of triacsin C and DHA were identified by performing flowcytometry and immunoblotting analysis. RESULTS: Combined treatment with DHA and triacsin C significantly induced apoptosis in RL95-2 endometrial carcinoma cells. Combined treatment with 125 μM DHA and 5 μM triacsin C significantly increased the sub-G1 population and apoptotic fragments in endometrial carcinoma cells. It was also demonstrated that DHA and triacsin C induced apoptosis through mitochondrial pathways via caspases-9, -3, and -7 as well as through the extrinsic pathway by activation of caspase-8/BID. CONCLUSIONS: Further elucidation of the apoptotic mechanisms involving DHA treatment with ACS ablation could shed light on possible new treatment strategies for endometrial cancer. In addition, further research into the mechanisms of DHA and triacsin C-induced apoptotic mechanisms may lead to the development of therapeutic strategies for endometrial cancer.
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spelling pubmed-100743232023-04-06 Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C Chung, Soo-Ho Lee, Hae-Hyeog Kim, Yeon-Suk Song, Kisung Kim, Tae-Hee Arch Med Sci Basic Research INTRODUCTION: Docosahexaenoic acid (DHA) supplementation has been reported to negatively correlate with cancer cell proliferation and tumour development in many cancer types. Although cumulative evidence has demonstrated the apoptotic effect and cytotoxicity of DHA against tumour development in many cell types, the precise cellular and biochemical mechanisms of DHA-induced apoptosis in human endometrial cancer cells have not been investigated. MATERIAL AND METHODS: MTT assay was performed to confirm the degree of apoptosis by combining treatment with DHA and triacsin C in endometrial cancer cell line. The synergistic effects of triacsin C and DHA were identified by performing flowcytometry and immunoblotting analysis. RESULTS: Combined treatment with DHA and triacsin C significantly induced apoptosis in RL95-2 endometrial carcinoma cells. Combined treatment with 125 μM DHA and 5 μM triacsin C significantly increased the sub-G1 population and apoptotic fragments in endometrial carcinoma cells. It was also demonstrated that DHA and triacsin C induced apoptosis through mitochondrial pathways via caspases-9, -3, and -7 as well as through the extrinsic pathway by activation of caspase-8/BID. CONCLUSIONS: Further elucidation of the apoptotic mechanisms involving DHA treatment with ACS ablation could shed light on possible new treatment strategies for endometrial cancer. In addition, further research into the mechanisms of DHA and triacsin C-induced apoptotic mechanisms may lead to the development of therapeutic strategies for endometrial cancer. Termedia Publishing House 2021-03-03 /pmc/articles/PMC10074323/ /pubmed/37034541 http://dx.doi.org/10.5114/aoms/111947 Text en Copyright: © 2021 Termedia & Banach https://creativecommons.org/licenses/by-nc-sa/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Basic Research
Chung, Soo-Ho
Lee, Hae-Hyeog
Kim, Yeon-Suk
Song, Kisung
Kim, Tae-Hee
Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C
title Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C
title_full Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C
title_fullStr Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C
title_full_unstemmed Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C
title_short Induction of apoptosis in RL95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin C
title_sort induction of apoptosis in rl95-2 human endometrial cancer cells by combination treatment with docosahexaenoic acid and triacsin c
topic Basic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10074323/
https://www.ncbi.nlm.nih.gov/pubmed/37034541
http://dx.doi.org/10.5114/aoms/111947
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