Micro RNA 100 sensitizes luminal A breast cancer cells to paclitaxel treatment in part by targeting mTOR
Luminal A breast cancer usually responds to hormonal therapies but does not benefit from chemotherapies, including microtubule-targeted paclitaxel. MicroRNAs could play a role in mediating this differential response. In this study, we examined the role of micro RNA 100 (miR-100) in the sensitivity o...
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Published in | Oncotarget Vol. 7; no. 5; pp. 5702 - 5714 |
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Abstract | Luminal A breast cancer usually responds to hormonal therapies but does not benefit from chemotherapies, including microtubule-targeted paclitaxel. MicroRNAs could play a role in mediating this differential response. In this study, we examined the role of micro RNA 100 (miR-100) in the sensitivity of breast cancer to paclitaxel treatment. We found that while miR-100 was downregulated in both human breast cancer primary tumors and cell lines, the degree of downregulation was greater in the luminal A subtype than in other subtypes. The IC
50
of paclitaxel was much higher in luminal A than in basal-like breast cancer cell lines. Ectopic miR-100 expression in the MCF-7 luminal A cell line enhanced the effect of paclitaxel on cell cycle arrest, multinucleation, and apoptosis, while knockdown of miR-100 in the MDA-MB-231 basal-like line compromised these effects. Similarly, overexpression of miR-100 enhanced the effects of paclitaxel on tumorigenesis in MCF-7 cells. Rapamycin-mediated inhibition of the mammalian target of rapamycin (mTOR), a target of miR-100, also sensitized MCF-7 cells to paclitaxel. Gene set enrichment analysis showed that genes that are part of the known paclitaxel-sensitive signature had a significant expression correlation with miR-100 in breast cancer samples. In addition, patients with lower levels of miR-100 expression had worse overall survival. These results suggest that miR-100 plays a causal role in determining the sensitivity of breast cancers to paclitaxel treatment. |
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AbstractList | Luminal A breast cancer usually responds to hormonal therapies but does not benefit from chemotherapies, including microtubule-targeted paclitaxel. MicroRNAs could play a role in mediating this differential response. In this study, we examined the role of micro RNA 100 (miR-100) in the sensitivity of breast cancer to paclitaxel treatment. We found that while miR-100 was downregulated in both human breast cancer primary tumors and cell lines, the degree of downregulation was greater in the luminal A subtype than in other subtypes. The IC
50
of paclitaxel was much higher in luminal A than in basal-like breast cancer cell lines. Ectopic miR-100 expression in the MCF-7 luminal A cell line enhanced the effect of paclitaxel on cell cycle arrest, multinucleation, and apoptosis, while knockdown of miR-100 in the MDA-MB-231 basal-like line compromised these effects. Similarly, overexpression of miR-100 enhanced the effects of paclitaxel on tumorigenesis in MCF-7 cells. Rapamycin-mediated inhibition of the mammalian target of rapamycin (mTOR), a target of miR-100, also sensitized MCF-7 cells to paclitaxel. Gene set enrichment analysis showed that genes that are part of the known paclitaxel-sensitive signature had a significant expression correlation with miR-100 in breast cancer samples. In addition, patients with lower levels of miR-100 expression had worse overall survival. These results suggest that miR-100 plays a causal role in determining the sensitivity of breast cancers to paclitaxel treatment. |
Author | Fu, Xing Zhang, Baotong He, Yuan Dong, Jin-Tang Fu, Li Zhu, Zhengmao Zhao, Ranran Fu, Liya |
AuthorAffiliation | 1 Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China 2 Emory Winship Cancer Institute, Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia, USA 3 Cancer Hospital of Tianjin Medical University, Tianjin, China |
AuthorAffiliation_xml | – name: 3 Cancer Hospital of Tianjin Medical University, Tianjin, China – name: 1 Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China – name: 2 Emory Winship Cancer Institute, Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia, USA |
Author_xml | – sequence: 1 givenname: Baotong surname: Zhang fullname: Zhang, Baotong organization: Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China, Emory Winship Cancer Institute, Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia, USA – sequence: 2 givenname: Ranran surname: Zhao fullname: Zhao, Ranran organization: Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China – sequence: 3 givenname: Yuan surname: He fullname: He, Yuan organization: Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China – sequence: 4 givenname: Xing surname: Fu fullname: Fu, Xing organization: Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China – sequence: 5 givenname: Liya surname: Fu fullname: Fu, Liya organization: Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China – sequence: 6 givenname: Zhengmao surname: Zhu fullname: Zhu, Zhengmao organization: Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China – sequence: 7 givenname: Li surname: Fu fullname: Fu, Li organization: Cancer Hospital of Tianjin Medical University, Tianjin, China – sequence: 8 givenname: Jin-Tang surname: Dong fullname: Dong, Jin-Tang organization: Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China, Emory Winship Cancer Institute, Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia, USA |
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Title | Micro RNA 100 sensitizes luminal A breast cancer cells to paclitaxel treatment in part by targeting mTOR |
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