MUC1 induces tamoxifen resistance in estrogen receptor-positive breast cancer
Introduction: Tamoxifen, as an essential therapeutic tool in the treatment of estrogen receptor-positive breast cancer, has been available for the past three decades and is currently being utilized as a chemo-preventive agent for patients at high risk for breast carcinoma. However, the induction of...
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| Published in: | Expert review of anticancer therapy Vol. 17; no. 7; pp. 607 - 613 |
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03-07-2017
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| Abstract | Introduction: Tamoxifen, as an essential therapeutic tool in the treatment of estrogen receptor-positive breast cancer, has been available for the past three decades and is currently being utilized as a chemo-preventive agent for patients at high risk for breast carcinoma. However, the induction of chemo-resistance during therapy has indicated a significant challenge with regards to this agent.
Areas covered: This review enumerates the role of MUC1-C proto-oncogene in tamoxifen resistance and describes a number of signaling pathways by which MUC1-C would mediate the development of resistance. Finally, recent clinical studies conducted on the magnitude of MUC1 in inducing tamoxifen resistance are described.
Expert commentary: Mucin 1, or MUC1, is aberrantly overexpressed on the entire tumor cell surface of most human cancers. Thus, it may result in the upregulation of several signaling pathways, such as growth cascades related to receptor tyrosine kinases (RTK), β-catenin and E-cadherin, as well as promoting gene transcription of Ras-related protein Rab-31 in order to mediate tumor growth control in response to tamoxifen. On the contrary, MUC1 suppresses apoptotic events, which in turn impresses upon cell fate. Also, it has been demonstrated that silencing MUC1-C proto-oncogene is associated with increased sensitivity to tamoxifen-induced growth inhibitors. |
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| AbstractList | Introduction: Tamoxifen, as an essential therapeutic tool in the treatment of estrogen receptor-positive breast cancer, has been available for the past three decades and is currently being utilized as a chemo-preventive agent for patients at high risk for breast carcinoma. However, the induction of chemo-resistance during therapy has indicated a significant challenge with regards to this agent.
Areas covered: This review enumerates the role of MUC1-C proto-oncogene in tamoxifen resistance and describes a number of signaling pathways by which MUC1-C would mediate the development of resistance. Finally, recent clinical studies conducted on the magnitude of MUC1 in inducing tamoxifen resistance are described.
Expert commentary: Mucin 1, or MUC1, is aberrantly overexpressed on the entire tumor cell surface of most human cancers. Thus, it may result in the upregulation of several signaling pathways, such as growth cascades related to receptor tyrosine kinases (RTK), β-catenin and E-cadherin, as well as promoting gene transcription of Ras-related protein Rab-31 in order to mediate tumor growth control in response to tamoxifen. On the contrary, MUC1 suppresses apoptotic events, which in turn impresses upon cell fate. Also, it has been demonstrated that silencing MUC1-C proto-oncogene is associated with increased sensitivity to tamoxifen-induced growth inhibitors. Tamoxifen, as an essential therapeutic tool in the treatment of estrogen receptor-positive breast cancer, has been available for the past three decades and is currently being utilized as a chemo-preventive agent for patients at high risk for breast carcinoma. However, the induction of chemo-resistance during therapy has indicated a significant challenge with regards to this agent. Areas covered: This review enumerates the role of MUC1-C proto-oncogene in tamoxifen resistance and describes a number of signaling pathways by which MUC1-C would mediate the development of resistance. Finally, recent clinical studies conducted on the magnitude of MUC1 in inducing tamoxifen resistance are described. Expert commentary: Mucin 1, or MUC1, is aberrantly overexpressed on the entire tumor cell surface of most human cancers. Thus, it may result in the upregulation of several signaling pathways, such as growth cascades related to receptor tyrosine kinases (RTK), β-catenin and E-cadherin, as well as promoting gene transcription of Ras-related protein Rab-31 in order to mediate tumor growth control in response to tamoxifen. On the contrary, MUC1 suppresses apoptotic events, which in turn impresses upon cell fate. Also, it has been demonstrated that silencing MUC1-C proto-oncogene is associated with increased sensitivity to tamoxifen-induced growth inhibitors. |
| Author | Merikhian, Parnaz Ghadirian, Reyhane Majidzadeh-A, Keivan Mansouri, Sepideh Farahmand, Leila |
| Author_xml | – sequence: 1 givenname: Parnaz surname: Merikhian fullname: Merikhian, Parnaz organization: Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR – sequence: 2 givenname: Reyhane surname: Ghadirian fullname: Ghadirian, Reyhane organization: Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR – sequence: 3 givenname: Leila surname: Farahmand fullname: Farahmand, Leila organization: Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR – sequence: 4 givenname: Sepideh surname: Mansouri fullname: Mansouri, Sepideh organization: Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR – sequence: 5 givenname: Keivan surname: Majidzadeh-A fullname: Majidzadeh-A, Keivan email: kmajidzadeh@razi.tums.ac.ir organization: Genetics Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR |
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| Snippet | Introduction: Tamoxifen, as an essential therapeutic tool in the treatment of estrogen receptor-positive breast cancer, has been available for the past three... Tamoxifen, as an essential therapeutic tool in the treatment of estrogen receptor-positive breast cancer, has been available for the past three decades and is... |
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| SubjectTerms | Antineoplastic Agents, Hormonal - administration & dosage Antineoplastic Agents, Hormonal - pharmacology Apoptosis - drug effects Breast Cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - pathology cancer progression Drug Resistance, Neoplasm - genetics estrogen receptor Female Gene Expression Regulation, Neoplastic Humans MUC1-C Mucin Mucin-1 - genetics Receptors, Estrogen - metabolism Signal Transduction - drug effects signaling pathways Tamoxifen - administration & dosage Tamoxifen - pharmacology Tamoxifen resistance development |
| Title | MUC1 induces tamoxifen resistance in estrogen receptor-positive breast cancer |
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