Reprogramming ovarian and breast cancer cells into non-cancerous cells by low-dose metformin or SN-38 through FOXO3 activation
Cancer is a leading cause of death worldwide. Because the cytotoxic effects of conventional chemotherapies often harm normal tissue cells along with cancer cells, conventional chemotherapies cause many unwanted or intolerable side effects. Thus, there is an unmet medical need to establish a paradigm...
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Published in | Scientific reports Vol. 4; no. 1; p. 5810 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
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Nature Publishing Group UK
24.07.2014
Nature Publishing Group |
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Abstract | Cancer is a leading cause of death worldwide. Because the cytotoxic effects of conventional chemotherapies often harm normal tissue cells along with cancer cells, conventional chemotherapies cause many unwanted or intolerable side effects. Thus, there is an unmet medical need to establish a paradigm of chemotherapy-induced differentiation of cancer cells with tolerable side effects. Here we show that low-dose metformin or SN-38 inhibits cell growth or survival in ovarian and breast cancer cells and suppresses their tumor growth
in vivo
. Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4 and c-Myc, in these cancer cells. This treatment also inhibits spheroid body-formation in 3-dimensional culture. In contrast, silencing FOXO3 diminishes all these cellular events when ovarian/breast cancer cells are treated with the mentioned drugs. These results suggest that low-dose metformin or SN-38 may reprogram these cancer cells into non-cancerous cells in a FOXO3-dependent manner and may allow patients to overcome these cancers with minimal side effects. |
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AbstractList | Cancer is a leading cause of death worldwide. Because the cytotoxic effects of conventional chemotherapies often harm normal tissue cells along with cancer cells, conventional chemotherapies cause many unwanted or intolerable side effects. Thus, there is an unmet medical need to establish a paradigm of chemotherapy-induced differentiation of cancer cells with tolerable side effects. Here we show that low-dose metformin or SN-38 inhibits cell growth or survival in ovarian and breast cancer cells and suppresses their tumor growth
in vivo
. Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4 and c-Myc, in these cancer cells. This treatment also inhibits spheroid body-formation in 3-dimensional culture. In contrast, silencing FOXO3 diminishes all these cellular events when ovarian/breast cancer cells are treated with the mentioned drugs. These results suggest that low-dose metformin or SN-38 may reprogram these cancer cells into non-cancerous cells in a FOXO3-dependent manner and may allow patients to overcome these cancers with minimal side effects. Cancer is a leading cause of death worldwide. Because the cytotoxic effects of conventional chemotherapies often harm normal tissue cells along with cancer cells, conventional chemotherapies cause many unwanted or intolerable side effects. Thus, there is an unmet medical need to establish a paradigm of chemotherapy-induced differentiation of cancer cells with tolerable side effects. Here we show that low-dose metformin or SN-38 inhibits cell growth or survival in ovarian and breast cancer cells and suppresses their tumor growth in vivo. Low-dose metformin or SN-38 increases FOXO3 nuclear localization as well as the amount of DNA damage markers and downregulates the expression of a cancer-stemness marker CD44 and other stemness markers, including Nanog, Oct-4, and c-Myc, in these cancer cells. This treatment also inhibits spheroid body-formation in 3-dimensional culture. In contrast, silencing FOXO3 diminishes all these cellular events when ovarian/breast cancer cells are treated with the mentioned drugs. These results suggest that low-dose metformin or SN-38 may reprogram these cancer cells into non-cancerous cells in a FOXO3-dependent manner, and may allow patients to overcome these cancers with minimal side effects. |
ArticleNumber | 5810 |
Author | Ma, Jessica Hu, Theodore Hu, Mickey C-T. Guan, Michelle Ma, Michael Chung, Young Min Berek, Jonathan S. |
Author_xml | – sequence: 1 givenname: Theodore surname: Hu fullname: Hu, Theodore organization: Division of Gynecologic Oncology, Department of Obstetrics & Gynecology, Stanford University School of Medicine – sequence: 2 givenname: Young Min surname: Chung fullname: Chung, Young Min organization: Division of Gynecologic Oncology, Department of Obstetrics & Gynecology, Stanford University School of Medicine – sequence: 3 givenname: Michelle surname: Guan fullname: Guan, Michelle organization: Division of Gynecologic Oncology, Department of Obstetrics & Gynecology, Stanford University School of Medicine – sequence: 4 givenname: Michael surname: Ma fullname: Ma, Michael organization: Division of Gynecologic Oncology, Department of Obstetrics & Gynecology, Stanford University School of Medicine – sequence: 5 givenname: Jessica surname: Ma fullname: Ma, Jessica organization: Division of Gynecologic Oncology, Department of Obstetrics & Gynecology, Stanford University School of Medicine – sequence: 6 givenname: Jonathan S. surname: Berek fullname: Berek, Jonathan S. organization: Division of Gynecologic Oncology, Department of Obstetrics & Gynecology, Stanford University School of Medicine – sequence: 7 givenname: Mickey C-T. surname: Hu fullname: Hu, Mickey C-T. organization: Division of Gynecologic Oncology, Department of Obstetrics & Gynecology, Stanford University School of Medicine |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25056111$$D View this record in MEDLINE/PubMed |
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Title | Reprogramming ovarian and breast cancer cells into non-cancerous cells by low-dose metformin or SN-38 through FOXO3 activation |
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