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      Methyl Antcinate A Suppresses the Population of Cancer Stem-Like Cells in MCF7 Human Breast Cancer Cell Line

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          Abstract

          Methyl antcinate A (MAA) is an ergostane-type triterpenoid extracted from the fruiting bodies of Antrodia camphorate that has been reported to be a cytotoxic agent towards some types of cancer cells, such as oral cancer and liver cancer. Cancer stem cells (CSCs) are a particular population within cancer cells which are responsible for tumor initiation, drug resistance and metastasis and targeting CSCs is an emerging area in cancer therapy. In this study, we examine the effect of MAA on cancer stem-like cells in the MCF7 human breast cancer cell line. Although MAA displayed very low cytotoxic effect towards MCF7 under normal culture conditions, it did show good inhibitory effects on the self-renewal capability which was examined by mammosphere culture including primary and secondary sphere. MAA also inhibited cell migration ability of MCF7 sphere cells. By western blot analysis, MAA was shown to suppress the expression of heat shock protein 27 and increase the expression of IκBα and p53. In conclusion, our data demonstrate that MAA has anti-CSC activity and is worthy of future development of potent anticancer agents.

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          The response of CD24(-/low)/CD44+ breast cancer-initiating cells to radiation.

          Tiffany Phillips, William H McBride, Frank Pajonk (2006)
          If cancer arises and is maintained by a small population of cancer-initiating cells within every tumor, understanding how these cells react to cancer treatment will facilitate improvement of cancer treatment in the future. Cancer-initiating cells can now be prospectively isolated from breast cancer cell lines and tumor samples and propagated as mammospheres in vitro under serum-free conditions. CD24(-/low)/CD44+ cancer-initiating cells were isolated from MCF-7 and MDA-MB-231 breast cancer monolayer cultures and propagated as mammospheres. Their response to radiation was investigated by assaying clonogenic survival and by measuring reactive oxygen species (ROS) levels, phosphorylation of the replacement histone H2AX, CD44 levels, CD24 levels, and Notch-1 activation using flow cytometry. All statistical tests were two-sided. Cancer-initiating cells were more resistant to radiation than cells grown as monolayer cultures (MCF-7: monolayer cultures, mean surviving fraction at 2 Gy [SF(2Gy)] = 0.2, versus mammospheres, mean SF(2Gy) = 0.46, difference = 0.26, 95% confidence interval [CI] = 0.05 to 0.47; P = .026; MDA-MB-231: monolayer cultures, mean SF(2Gy) = 0.5, versus mammospheres, mean SF(2Gy) = 0.69, difference = 0.19, 95% CI = -0.07 to 0.45; P = .09). Levels of ROS increased in both mammospheres and monolayer cultures after irradiation with a single dose of 10 Gy but were lower in mammospheres than in monolayer cultures (MCF-7 monolayer cultures: 0 Gy, mean = 1.0, versus 10 Gy, mean = 3.32, difference = 2.32, 95% CI = 0.67 to 3.98; P = .026; mammospheres: 0 Gy, mean = 0.58, versus 10 Gy, mean = 1.46, difference = 0.88, 95% CI = 0.20 to 1.56; P = .031); phosphorylation of H2AX increased in irradiated monolayer cultures, but no change was observed in mammospheres. Fractionated doses of irradiation increased activation of Notch-1 (untreated, mean = 10.7, versus treated, mean = 15.1, difference = 4.4, 95% CI = 2.7 to 6.1, P = .002) and the percentage of the cancer stem/initiating cells in the nonadherent cell population of MCF-7 monolayer cultures (untreated, mean = 3.52%, versus treated, mean = 7.5%, difference = 3.98%, 95% CI = 1.67% to 6.25%, P = .009). Breast cancer-initiating cells are a relatively radioresistant subpopulation of breast cancer cells and increase in numbers after short courses of fractionated irradiation. These findings offer a possible mechanism for the accelerated repopulation of tumor cells observed during gaps in radiotherapy.
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            The tumor suppressor p53 regulates polarity of self-renewing divisions in mammary stem cells.

            Angelo Cicalese, Giuseppina Bonizzi, Cristina Pasi … (2009)
            Stem-like cells may be integral to the development and maintenance of human cancers. Direct proof is still lacking, mainly because of our poor understanding of the biological differences between normal and cancer stem cells (SCs). Using the ErbB2 transgenic model of breast cancer, we found that self-renewing divisions of cancer SCs are more frequent than their normal counterparts, unlimited and symmetric, thus contributing to increasing numbers of SCs in tumoral tissues. SCs with targeted mutation of the tumor suppressor p53 possess the same self-renewal properties as cancer SCs, and their number increases progressively in the p53 null premalignant mammary gland. Pharmacological reactivation of p53 correlates with restoration of asymmetric divisions in cancer SCs and tumor growth reduction, without significant effects on additional cancer cells. These data demonstrate that p53 regulates polarity of cell division in mammary SCs and suggest that loss of p53 favors symmetric divisions of cancer SCs, contributing to tumor growth.
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              Heat shock proteins in cancer: diagnostic, prognostic, predictive, and treatment implications

              Daniel Ciocca, Stuart K. Calderwood (2005)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Molecules
                Journal ID (iso-abbrev): Molecules
                Journal ID (publisher-id): molecules
                Title: Molecules
                Publisher: MDPI
                ISSN (Electronic): 1420-3049
                Publication date (Electronic): 26 February 2013
                Publication date Collection: March 2013
                Volume: 18
                Issue: 3
                Pages: 2539-2548
                Affiliations
                [1 ]School of Dentistry, Chung Shan Medical University, Taichung 402, Taiwan; E-Mails: cyp@ 123456csmu.edu.tw (C.-Y.P.); ccyu@ 123456csmu.edu.tw (C.-C.Y.)
                [2 ]Department of Dentistry, Chung Shan Medical University Hospital, Taichung 402, Taiwan
                [3 ]Department of Biomedical Sciences, Chung Shan Medical University, Taichung 402, Taiwan; E-Mail: chungfongpin@ 123456hotmail.com
                [4 ]Institute of Oral Science, Chung Shan Medical University, Taichung 402, Taiwan
                [5 ]Department of Medical Laboratory Science and Biotechnology, Kaohsiung Medical University, Kaohsiung 807, Taiwan; E-Mail: wanchi@ 123456kmu.edu.tw
                [6 ]Department of Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan
                [7 ]Institute of Biochemical Sciences and Technology, Chaoyang University of Technology, Taichung 413, Taiwan; E-Mail: ymtzeng@ 123456cyut.edu.tw
                [8 ]Department of Medical Research, Chung Shan Medical University Hospital, Taichung 402, Taiwan
                Author notes
                [* ] Author to whom correspondence should be addressed; E-Mail: changww@ 123456csmu.edu.tw ; Tel.: +886-4-2473-0022 (ext.12317); Fax: +886-4-2324-8187.
                Article
                Publisher ID: molecules-18-02539
                DOI: 10.3390/molecules18032539
                PMC ID: 6270214
                PubMed ID: 23442930
                SO-VID: f7432777-da9f-4623-ae51-21e2cdb8947c
                Copyright © © 2013 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 12 December 2012
                Date revision received : 22 January 2013
                Date accepted : 19 February 2013
                Categories
                Subject: Article

                Keywords: methyl antcinate a,breast cancer stem-like cells,p53,hsp27,iκbα
                Data availability:
                Keywords: methyl antcinate a, breast cancer stem-like cells, p53, hsp27, iκbα

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