Down-regulation of Myeloid Cell Leukemia-1 through Inhibiting Erk/Pin 1 Pathway by Sorafenib Facilitates Chemosensitization in Breast Cancer
Myeloid cell leukemia-1 (Mcl-1), a Bcl-2–like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human malignancies. A peptidyl-prolyl cis/trans isomerase, Pin1 is involved in many cellular events, such as cell cycle progression, cell proliferation, and di...
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| Published in | Cancer research (Chicago, Ill.) Vol. 68; no. 15; pp. 6109 - 6117 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.08.2008
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Myeloid cell leukemia-1 (Mcl-1), a Bcl-2–like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human malignancies. A peptidyl-prolyl cis/trans isomerase, Pin1 is involved in many cellular events, such as cell cycle progression, cell proliferation, and differentiation through isomerizing prophosphorylated substrates. It has been reported that down-regulation of Pin1 induces apoptosis, and that Erk phosphorylates and up-regulates Mcl-1; however, the underlying mechanisms for the two phenomena are not clear yet. Here, we showed that Pin 1 stabilizes Mcl-1, which is required for Mcl-1 posphorylation by Erk. First, we found expression of Mcl-1 and Pin1 were positively correlated and associated with poor survival in human breast cancer. We then showed that Erk could phosphorylate Mcl-1 at two consensus residues, Thr 92 and 163, which is required for the association of Mcl-1 and Pin1, resulting in stabilization of Mcl-1. Moreover, Pin1 is also required for the up-regulation of Mcl-1 by Erk activation. Based on this newly identified mechanism of Mcl-1 stabilization, two strategies were used to overcome Mcl-1–mediated chemoresistance: inhibiting Erk by Sorafenib, an approved clinical anticancer drug, or knocking down Pin1 by using a SiRNA technique. In conclusion, the current report not only unravels a novel mechanism to link Erk/Pin1 pathway and Mcl-1–mediated chemoresistance but also provides a plausible combination therapy, Taxol (Paclitaxel) plus Sorafenib, which was shown to be effective in killing breast cancer cells. [Cancer Res 2008;68(15):6109–17] |
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| AbstractList | Myeloid cell leukemia-1 (Mcl-1), a Bcl-2-like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human malignancies. A peptidyl-prolyl cis/trans isomerase, Pin1 is involved in many cellular events, such as cell cycle progression, cell proliferation, and differentiation through isomerizing prophosphorylated substrates. It has been reported that down-regulation of Pin1 induces apoptosis, and that Erk phosphorylates and up-regulates Mcl-1; however, the underlying mechanisms for the two phenomena are not clear yet. Here, we showed that Pin 1 stabilizes Mcl-1, which is required for Mcl-1 posphorylation by Erk. First, we found expression of Mcl-1 and Pin1 were positively correlated and associated with poor survival in human breast cancer. We then showed that Erk could phosphorylate Mcl-1 at two consensus residues, Thr 92 and 163, which is required for the association of Mcl-1 and Pin1, resulting in stabilization of Mcl-1. Moreover, Pin1 is also required for the up-regulation of Mcl-1 by Erk activation. Based on this newly identified mechanism of Mcl-1 stabilization, two strategies were used to overcome Mcl-1-mediated chemoresistance: inhibiting Erk by Sorafenib, an approved clinical anticancer drug, or knocking down Pin1 by using a SiRNA technique. In conclusion, the current report not only unravels a novel mechanism to link Erk/Pin1 pathway and Mcl-1-mediated chemoresistance but also provides a plausible combination therapy, Taxol (Paclitaxel) plus Sorafenib, which was shown to be effective in killing breast cancer cells. Myeloid cell leukemia-1 (Mcl-1), a Bcl-2-like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human malignancies. A peptidyl-prolyl cis/trans isomerase, Pin1 is involved in many cellular events, such as cell cycle progression, cell proliferation, and differentiation through isomerizing prophosphorylated substrates. It has been reported that down-regulation of Pin1 induces apoptosis, and that Erk phosphorylates and up-regulates Mcl-1; however, the underlying mechanisms for the two phenomena are not clear yet. Here, we showed that Pin 1 stabilizes Mcl-1, which is required for Mcl-1 posphorylation by Erk. First, we found expression of Mcl-1 and Pin1 were positively correlated and associated with poor survival in human breast cancer. We then showed that Erk could phosphorylate Mcl-1 at two consensus residues, Thr 92 and 163, which is required for the association of Mcl-1 and Pin1, resulting in stabilization of Mcl-1. Moreover, Pin1 is also required for the up-regulation of Mcl-1 by Erk activation. Based on this newly identified mechanism of Mcl-1 stabilization, two strategies were used to overcome Mcl-1-mediated chemoresistance: inhibiting Erk by Sorafenib, an approved clinical anticancer drug, or knocking down Pin1 by using a SiRNA technique. In conclusion, the current report not only unravels a novel mechanism to link Erk/Pin1 pathway and Mcl-1-mediated chemoresistance but also provides a plausible combination therapy, Taxol (Paclitaxel) plus Sorafenib, which was shown to be effective in killing breast cancer cells.Myeloid cell leukemia-1 (Mcl-1), a Bcl-2-like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human malignancies. A peptidyl-prolyl cis/trans isomerase, Pin1 is involved in many cellular events, such as cell cycle progression, cell proliferation, and differentiation through isomerizing prophosphorylated substrates. It has been reported that down-regulation of Pin1 induces apoptosis, and that Erk phosphorylates and up-regulates Mcl-1; however, the underlying mechanisms for the two phenomena are not clear yet. Here, we showed that Pin 1 stabilizes Mcl-1, which is required for Mcl-1 posphorylation by Erk. First, we found expression of Mcl-1 and Pin1 were positively correlated and associated with poor survival in human breast cancer. We then showed that Erk could phosphorylate Mcl-1 at two consensus residues, Thr 92 and 163, which is required for the association of Mcl-1 and Pin1, resulting in stabilization of Mcl-1. Moreover, Pin1 is also required for the up-regulation of Mcl-1 by Erk activation. Based on this newly identified mechanism of Mcl-1 stabilization, two strategies were used to overcome Mcl-1-mediated chemoresistance: inhibiting Erk by Sorafenib, an approved clinical anticancer drug, or knocking down Pin1 by using a SiRNA technique. In conclusion, the current report not only unravels a novel mechanism to link Erk/Pin1 pathway and Mcl-1-mediated chemoresistance but also provides a plausible combination therapy, Taxol (Paclitaxel) plus Sorafenib, which was shown to be effective in killing breast cancer cells. Myeloid cell leukemia-1 (Mcl-1), a Bcl-2–like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human malignancies. A peptidyl-prolyl cis/trans isomerase, Pin1 is involved in many cellular events, such as cell cycle progression, cell proliferation, and differentiation through isomerizing prophosphorylated substrates. It has been reported that down-regulation of Pin1 induces apoptosis, and that Erk phosphorylates and up-regulates Mcl-1; however, the underlying mechanisms for the two phenomena are not clear yet. Here, we showed that Pin 1 stabilizes Mcl-1, which is required for Mcl-1 posphorylation by Erk. First, we found expression of Mcl-1 and Pin1 were positively correlated and associated with poor survival in human breast cancer. We then showed that Erk could phosphorylate Mcl-1 at two consensus residues, Thr 92 and 163, which is required for the association of Mcl-1 and Pin1, resulting in stabilization of Mcl-1. Moreover, Pin1 is also required for the up-regulation of Mcl-1 by Erk activation. Based on this newly identified mechanism of Mcl-1 stabilization, two strategies were used to overcome Mcl-1–mediated chemoresistance: inhibiting Erk by Sorafenib, an approved clinical anticancer drug, or knocking down Pin1 by using a SiRNA technique. In conclusion, the current report not only unravels a novel mechanism to link Erk/Pin1 pathway and Mcl-1–mediated chemoresistance but also provides a plausible combination therapy, Taxol (Paclitaxel) plus Sorafenib, which was shown to be effective in killing breast cancer cells. [Cancer Res 2008;68(15):6109–17] |
| Author | Yen, Chia-Jui Li, Long-Yuan Ding, Qingqing Lin, Chun-Yi Hung, Mien-Chie Huo, Longfei Chen, Yun-Ju Rita Lee, Dung-Fang Tsai, Chang-Hai Liao, Yong Tsai, Fuu-Jen Yang, Jer-Yen Hsu, Jung-Mao Wei, Yongkun Xia, Weiya Yang, Yan Lai, Chien-Chen Chang, Chun-Ju Kuo, Hsu-Ping |
| AuthorAffiliation | 7 Asia University, Taichung, Taiwan 3 Graduate School of Biomedical Sciences, The University of Texas, Houston, Texas 1 Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 2 Department of Molecular Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 5 China Medical University and Hospital, Taichung, Taiwan 4 Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan 6 Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University and Hospital; Taichung, Taiwan |
| AuthorAffiliation_xml | – name: 7 Asia University, Taichung, Taiwan – name: 3 Graduate School of Biomedical Sciences, The University of Texas, Houston, Texas – name: 4 Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan – name: 1 Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas – name: 5 China Medical University and Hospital, Taichung, Taiwan – name: 6 Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University and Hospital; Taichung, Taiwan – name: 2 Department of Molecular Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas |
| Author_xml | – sequence: 1 givenname: Qingqing surname: Ding fullname: Ding, Qingqing – sequence: 2 givenname: Longfei surname: Huo fullname: Huo, Longfei – sequence: 3 givenname: Jer-Yen surname: Yang fullname: Yang, Jer-Yen – sequence: 4 givenname: Weiya surname: Xia fullname: Xia, Weiya – sequence: 5 givenname: Yongkun surname: Wei fullname: Wei, Yongkun – sequence: 6 givenname: Yong surname: Liao fullname: Liao, Yong – sequence: 7 givenname: Chun-Ju surname: Chang fullname: Chang, Chun-Ju – sequence: 8 givenname: Yan surname: Yang fullname: Yang, Yan – sequence: 9 givenname: Chien-Chen surname: Lai fullname: Lai, Chien-Chen – sequence: 10 givenname: Dung-Fang surname: Lee fullname: Lee, Dung-Fang – sequence: 11 givenname: Chia-Jui surname: Yen fullname: Yen, Chia-Jui – sequence: 12 givenname: Yun-Ju Rita surname: Chen fullname: Chen, Yun-Ju Rita – sequence: 13 givenname: Jung-Mao surname: Hsu fullname: Hsu, Jung-Mao – sequence: 14 givenname: Hsu-Ping surname: Kuo fullname: Kuo, Hsu-Ping – sequence: 15 givenname: Chun-Yi surname: Lin fullname: Lin, Chun-Yi – sequence: 16 givenname: Fuu-Jen surname: Tsai fullname: Tsai, Fuu-Jen – sequence: 17 givenname: Long-Yuan surname: Li fullname: Li, Long-Yuan – sequence: 18 givenname: Chang-Hai surname: Tsai fullname: Tsai, Chang-Hai – sequence: 19 givenname: Mien-Chie surname: Hung fullname: Hung, Mien-Chie |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18676833$$D View this record in MEDLINE/PubMed |
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| PublicationTitle | Cancer research (Chicago, Ill.) |
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| Snippet | Myeloid cell leukemia-1 (Mcl-1), a Bcl-2–like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human... Myeloid cell leukemia-1 (Mcl-1), a Bcl-2-like antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human... |
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| SubjectTerms | Antineoplastic Agents - pharmacology Benzenesulfonates - pharmacology Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Line, Tumor Down-Regulation Humans MAP Kinase Signaling System Mutagenesis, Site-Directed Myeloid Cell Leukemia Sequence 1 Protein Niacinamide - analogs & derivatives NIMA-Interacting Peptidylprolyl Isomerase Peptidylprolyl Isomerase - metabolism Phenylurea Compounds Phosphorylation Proto-Oncogene Proteins c-bcl-2 - physiology Pyridines - pharmacology Sorafenib |
| Title | Down-regulation of Myeloid Cell Leukemia-1 through Inhibiting Erk/Pin 1 Pathway by Sorafenib Facilitates Chemosensitization in Breast Cancer |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/18676833 https://www.proquest.com/docview/69377691 https://pubmed.ncbi.nlm.nih.gov/PMC2676572 |
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