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Aspisol inhibits tumor growth and induces apoptosis in breast cancer

Aspisol inhibits tumor growth and induces apoptosis in breast cancer

Nonsteroidal anti-inflammatory drugs inhibit cell proliferation and induce apoptosis in various cancer cell lines, which is considered to be an important mechanism for their anti-tumor activity and cancer prevention. However, the molecular mechanisms through which these compounds induce apoptosis ar...

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Main Authors: Zhu, X.G., Tao, L., Mei, Z.R., Wu, H.P., Jiang, Z.W.
Format: Article
Language:English
Published: Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України 2008
Series:Experimental Oncology
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Original contributions
Online Access:http://dspace.nbuv.gov.ua/handle/123456789/139930
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spelling irk-123456789-1399302018-06-22T03:04:38Z Aspisol inhibits tumor growth and induces apoptosis in breast cancer Zhu, X.G. Tao, L. Mei, Z.R. Wu, H.P. Jiang, Z.W. Original contributions Nonsteroidal anti-inflammatory drugs inhibit cell proliferation and induce apoptosis in various cancer cell lines, which is considered to be an important mechanism for their anti-tumor activity and cancer prevention. However, the molecular mechanisms through which these compounds induce apoptosis are not well understood. Aim: to determine the effects of nonselective cyclooxygenase-2 (COX-2) inhibitor, aspisol on breast cancer cells in vitro and in vivo. Methods: The cytotoxic activity of aspisol was evaluated by MTT assay. The apoptosis index of cells was measured by flow cytometry. Immunohistochemical staining was used to detect expressions of COX-2 and caspase-3 in MDA-MB-231 cells. The expression of bcl-2 and bax was analyzed by Western blot analysis. The content of prostaglandin E2 (PGE2) in MDA-MB-231 cells was estimated by ELISA. In vivo apoptosis of the tumor cells was detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). Results: Our results showed that aspisol reduced viability of MDA-MB-231 cells in time- and dose- dependent fashions and induced apoptosis by increase of caspase-3 and bax expressions while decrease of COX-2 and bcl-2 expression in vitro. In addition, exposure to aspisol decreased the basal release of PGE2. In vivo, aspisol also inhibited the proliferation of breast cancer cells and induced their apoptosis. Conclusions: Our in vitro and in vivo data indicated that the antitumor effects of aspisol on breast cancer cells was probably mediated by the induction of apoptosis, and it could be linked to the downregulation of the COX-2 or bcl-2 expression and up-regulation of caspase-3 or bax expression. Нестероидные противовоспалительные препараты ингибируют пролиферацию клеток и вызывают апоптоз во многих опухолевых клеточных линиях, что считается важным механизмом их противоопухолевой активности и профилактики развития рака. Тем не менее молекулярные механизмы апоптотического действия этих препаратов изучены недостаточно. Цель: изучить действие неспецифического ингибитора циклогексиназы-2 (COX-2) — аспизола — на злокачественные клетки рака молочной железы in vitro и in vivo. Методы: выживаемоть клеток MDA-MB-231 определяли с помощью MTT-теста. Апоптотический индекс измеряли с помощью проточной цитометрии и иммуногистохимическим окрашиванием с антителами против COX-2 и каспазы-3. Экспрессию bcl-2 и bax изучали с помощью Вестерн-блот-анализа. Содержание простагландина E2 (PGE2 ) в клетках MDA-MB-231 оценивали методом ELISA. In vivo апоптоз опухолевых клеток определяли путем выявления разрывов ДНК с помощью концевой дезоксинуклеот-идилтранферазы (метод TUNEL). Результаты: показано, что в зависимости от времени инкубации и дозы аспизол угнетал рост клеток MDA-MB-231 in vitro и вызывал их апоптоз на фоне повышения экспрессии каспазы-3 и bax, а также снижения экспрессии COX-2 и bcl-2. В условиях in vivo аспизол также ингибировал пролиферацию злокачественных клеток рака молочной железы и вызывал их апоптоз. Выводы: данные, полученные in vitro и in vivo, свидетельствуют о противоопухолевом эффекте аспизола на клетки рака молочной железы, что скорее всего опосредовано его проапоптотическим действием и может быть связано со снижением экспрессии COX-2 и bcl-2, а также повышением экспрессии каспазы-3 и bax. 2008 Article Aspisol inhibits tumor growth and induces apoptosis in breast cancer / X.G. Zhu, L. Tao, Z.R. Mei, H.P. Wu, Z.W. Jiang // Experimental Oncology. — 2008. — Т. 30, № 4. — С. 289–294. — Бібліогр.: 25 назв. — англ. 1812-9269 http://dspace.nbuv.gov.ua/handle/123456789/139930 en Experimental Oncology Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України
institution Digital Library of Periodicals of National Academy of Sciences of Ukraine
collection DSpace DC
language English
topic Original contributions
Original contributions
spellingShingle Original contributions
Original contributions
Zhu, X.G.
Tao, L.
Mei, Z.R.
Wu, H.P.
Jiang, Z.W.
Aspisol inhibits tumor growth and induces apoptosis in breast cancer
Experimental Oncology
description Nonsteroidal anti-inflammatory drugs inhibit cell proliferation and induce apoptosis in various cancer cell lines, which is considered to be an important mechanism for their anti-tumor activity and cancer prevention. However, the molecular mechanisms through which these compounds induce apoptosis are not well understood. Aim: to determine the effects of nonselective cyclooxygenase-2 (COX-2) inhibitor, aspisol on breast cancer cells in vitro and in vivo. Methods: The cytotoxic activity of aspisol was evaluated by MTT assay. The apoptosis index of cells was measured by flow cytometry. Immunohistochemical staining was used to detect expressions of COX-2 and caspase-3 in MDA-MB-231 cells. The expression of bcl-2 and bax was analyzed by Western blot analysis. The content of prostaglandin E2 (PGE2) in MDA-MB-231 cells was estimated by ELISA. In vivo apoptosis of the tumor cells was detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). Results: Our results showed that aspisol reduced viability of MDA-MB-231 cells in time- and dose- dependent fashions and induced apoptosis by increase of caspase-3 and bax expressions while decrease of COX-2 and bcl-2 expression in vitro. In addition, exposure to aspisol decreased the basal release of PGE2. In vivo, aspisol also inhibited the proliferation of breast cancer cells and induced their apoptosis. Conclusions: Our in vitro and in vivo data indicated that the antitumor effects of aspisol on breast cancer cells was probably mediated by the induction of apoptosis, and it could be linked to the downregulation of the COX-2 or bcl-2 expression and up-regulation of caspase-3 or bax expression.
format Article
author Zhu, X.G.
Tao, L.
Mei, Z.R.
Wu, H.P.
Jiang, Z.W.
author_facet Zhu, X.G.
Tao, L.
Mei, Z.R.
Wu, H.P.
Jiang, Z.W.
author_sort Zhu, X.G.
title Aspisol inhibits tumor growth and induces apoptosis in breast cancer
title_short Aspisol inhibits tumor growth and induces apoptosis in breast cancer
title_full Aspisol inhibits tumor growth and induces apoptosis in breast cancer
title_fullStr Aspisol inhibits tumor growth and induces apoptosis in breast cancer
title_full_unstemmed Aspisol inhibits tumor growth and induces apoptosis in breast cancer
title_sort aspisol inhibits tumor growth and induces apoptosis in breast cancer
publisher Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України
publishDate 2008
topic_facet Original contributions
url http://dspace.nbuv.gov.ua/handle/123456789/139930
citation_txt Aspisol inhibits tumor growth and induces apoptosis in breast cancer / X.G. Zhu, L. Tao, Z.R. Mei, H.P. Wu, Z.W. Jiang // Experimental Oncology. — 2008. — Т. 30, № 4. — С. 289–294. — Бібліогр.: 25 назв. — англ.
series Experimental Oncology
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first_indexed 2023-10-18T21:21:26Z
last_indexed 2023-10-18T21:21:26Z
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