26
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Silibinin Enhances Ultraviolet B-Induced Apoptosis in MCF-7 Human Breast Cancer Cells

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Purpose

          Chemotherapies for breast cancer generally have strong cellular cytotoxicity and severe side effects. Thus, significant emphasis has been placed on combinations of naturally occurring chemopreventive agents. Silibinin is a major bioactive flavonolignan extracted from milk thistle with chemopreventive activity in various organs including the skin, prostate, and breast. However, the mechanism underlying the inhibitory action of silibinin in breast cancer has not been completely elucidated. Therefore, we investigated the effect of silibinin in MCF-7 human breast cancer cells and determined whether silibinin enhances ultraviolet (UV) B-induced apoptosis.

          Methods

          The effects of silibinin on MCF-7 cell viability were determined using the MTT assay. The effect of silibinin on PARP cleavage, as the hallmark of apoptotic cell death, and p53 protein expression in MCF-7 cells was analyzed using Western blot. The effect of silibinin on UVB-induced apoptosis in MCF-7 cells was analyzed by flow cytometry.

          Results

          A dose- and time-dependent reduction in viability was observed in MCF-7 cells treated with silibinin. Silibinin strongly induced apoptotic cell death in MCF-7 cells, and induction of apoptosis was associated with increased p53 expression. Moreover, silibinin enhanced UVB-induced apoptosis in MCF-7 cells.

          Conclusion

          Silibinin induced a loss of cell viability and apoptotic cell death in MCF-7 cells. Furthermore, the combination of silibinin and UVB resulted in an additive effect on apoptosis in MCF-7 cells. These results suggest that silibinin might be an important supplemental agent for treating patients with breast cancer.

          Related collections

          Most cited references28

          • Record: found
          • Abstract: found
          • Article: not found

          The p53 proto-oncogene can act as a suppressor of transformation.

          DNA clones of the wild-type p53 proto-oncogene inhibit the ability of E1A plus ras or mutant p53 plus ras-activated oncogenes to transform primary rat embryo fibroblasts. The rare clones of transformed foci that result from E1A plus ras plus wild-type p53 triple transfections all contain the p53 DNA in their genome, but the great majority fail to express the p53 protein. The three cell lines derived from such foci that express p53 all produce mutant p53 proteins with properties similar or identical to transformation-activated p53 proteins. The p53 mutants selected in this fashion (transformation in vitro) resemble the p53 mutants selected in tumors (in vivo). These results suggest that the p53 proto-oncogene can act negatively to block transformation.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Apoptosis in cancer.

            In the last decade, basic cancer research has produced remarkable advances in our understanding of cancer biology and cancer genetics. Among the most important of these advances is the realization that apoptosis and the genes that control it have a profound effect on the malignant phenotype. For example, it is now clear that some oncogenic mutations disrupt apoptosis, leading to tumor initiation, progression or metastasis. Conversely, compelling evidence indicates that other oncogenic changes promote apoptosis, thereby producing selective pressure to override apoptosis during multistage carcinogenesis. Finally, it is now well documented that most cytotoxic anticancer agents induce apoptosis, raising the intriguing possibility that defects in apoptotic programs contribute to treatment failure. Because the same mutations that suppress apoptosis during tumor development also reduce treatment sensitivity, apoptosis provides a conceptual framework to link cancer genetics with cancer therapy. An intense research effort is uncovering the underlying mechanisms of apoptosis such that, in the next decade, one envisions that this information will produce new strategies to exploit apoptosis for therapeutic benefit.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              Mechanisms and functions of cell death.

                Bookmark

                Author and article information

                Journal
                J Breast Cancer
                JBC
                Journal of Breast Cancer
                Korean Breast Cancer Society
                1738-6756
                2092-9900
                March 2011
                31 March 2011
                : 14
                : 1
                : 8-13
                Affiliations
                Department of Biochemistry, Institute for Medical Sciences, Chonbuk National University Medical School, Jeonju, Korea.
                [1 ]Division of Breast · Thyroid Surgery, Department of Surgery, Chonbuk National University Medical School, Jeonju, Korea.
                Author notes
                Correspondence: Sung Hoo Jung. Division of Breast · Thyroid Surgery, Department of Surgery, Chonbuk National University Medical School, 634-18 Geumam-dong, Deokjin-gu, Jeonju 561-180, Korea. Tel: +82-63-250-2133, Fax: +82-63-271-6197, shjung@ 123456jbnu.ac.kr

                *These authors equally contributed to this study.

                Article
                10.4048/jbc.2011.14.1.8
                3148510
                21847388
                d80ed3c1-9d99-40d9-969c-6063c11ecf9d
                © 2011 Korean Breast Cancer Society

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 April 2010
                : 21 December 2010
                Categories
                Original Article

                Oncology & Radiotherapy
                apoptosis,mcf-7,ultraviolet b,p53,silibinin
                Oncology & Radiotherapy
                apoptosis, mcf-7, ultraviolet b, p53, silibinin

                Comments

                Comment on this article