p53 Attenuates the oncogenic Ras-induced epithelial–mesenchymal transition in human mammary epithelial cells
•Increased expression of p53 reversed the EMT phenotype.•Restoration of p53 expression suppressed EMT-mediated stem cell phenotype.•Enhanced expression of p53 reduced the oncogenic Ras-induced tumor growth of human mammary epithelial cells.•p53 downregulated the oncogenic Ras-induced signaling pathw...
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| Published in | Biochemical and biophysical research communications Vol. 434; no. 3; pp. 606 - 613 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
10.05.2013
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| Abstract | •Increased expression of p53 reversed the EMT phenotype.•Restoration of p53 expression suppressed EMT-mediated stem cell phenotype.•Enhanced expression of p53 reduced the oncogenic Ras-induced tumor growth of human mammary epithelial cells.•p53 downregulated the oncogenic Ras-induced signaling pathways.
Inactivation of the tumor suppressor p53 and activation of the oncogene Ras are the two most pivotal events in tumor development. However, potential intersection between p53 and Ras activity during an EMT process, which plays a crucial role during malignant tumor progression, remains elusive. Here, we report that increased expression of wild type p53 suppressed H-RasV12-induced EMT phenotypes and restrained stem cell properties, through downregulation of MEK-ERK signaling pathways. In vivo experiments showed that p53 was able to inhibit H-RasV12-induced tumor growth of human mammary epithelial cells. This study elucidates a novel correlation between the tumor suppressor gene p53 and the oncogene Ras in regulating EMT program, and expands the knowledge about the function of p53 in EMT process. |
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| AbstractList | Inactivation of the tumor suppressor p53 and activation of the oncogene Ras are the two most pivotal events in tumor development. However, potential intersection between p53 and Ras activity during an EMT process, which plays a crucial role during malignant tumor progression, remains elusive. Here, we report that increased expression of wild type p53 suppressed H-Ras(V12)-induced EMT phenotypes and restrained stem cell properties, through downregulation of MEK-ERK signaling pathways. In vivo experiments showed that p53 was able to inhibit H-Ras(V12)-induced tumor growth of human mammary epithelial cells. This study elucidates a novel correlation between the tumor suppressor gene p53 and the oncogene Ras in regulating EMT program, and expands the knowledge about the function of p53 in EMT process. •Increased expression of p53 reversed the EMT phenotype.•Restoration of p53 expression suppressed EMT-mediated stem cell phenotype.•Enhanced expression of p53 reduced the oncogenic Ras-induced tumor growth of human mammary epithelial cells.•p53 downregulated the oncogenic Ras-induced signaling pathways. Inactivation of the tumor suppressor p53 and activation of the oncogene Ras are the two most pivotal events in tumor development. However, potential intersection between p53 and Ras activity during an EMT process, which plays a crucial role during malignant tumor progression, remains elusive. Here, we report that increased expression of wild type p53 suppressed H-RasV12-induced EMT phenotypes and restrained stem cell properties, through downregulation of MEK-ERK signaling pathways. In vivo experiments showed that p53 was able to inhibit H-RasV12-induced tumor growth of human mammary epithelial cells. This study elucidates a novel correlation between the tumor suppressor gene p53 and the oncogene Ras in regulating EMT program, and expands the knowledge about the function of p53 in EMT process. |
| Author | Huang, Baiqu Liang, Qian Feng, Jingxin Zhang, Yu Li, Lili Hou, Pingfu Lu, Jun Lei, Yang Han, Liping Zhang, Jianchao Gao, Xiaoge |
| Author_xml | – sequence: 1 givenname: Jianchao surname: Zhang fullname: Zhang, Jianchao organization: The Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, PR China – sequence: 2 givenname: Yang surname: Lei fullname: Lei, Yang organization: The Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, PR China – sequence: 3 givenname: Xiaoge surname: Gao fullname: Gao, Xiaoge organization: The Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, PR China – sequence: 4 givenname: Qian surname: Liang fullname: Liang, Qian organization: The Key Laboratory of Molecular Epigenetics of Ministry of Education (MOE), Northeast Normal University, Changchun 130024, PR China – sequence: 5 givenname: Lili surname: Li fullname: Li, Lili organization: The Key Laboratory of Molecular Epigenetics of Ministry of Education (MOE), Northeast Normal University, Changchun 130024, PR China – sequence: 6 givenname: Jingxin surname: Feng fullname: Feng, Jingxin organization: The Key Laboratory of Molecular Epigenetics of Ministry of Education (MOE), Northeast Normal University, Changchun 130024, PR China – sequence: 7 givenname: Pingfu surname: Hou fullname: Hou, Pingfu organization: The Key Laboratory of Molecular Epigenetics of Ministry of Education (MOE), Northeast Normal University, Changchun 130024, PR China – sequence: 8 givenname: Liping surname: Han fullname: Han, Liping organization: School of Life Sciences, Changchun Normal University, Changchun 130032, PR China – sequence: 9 givenname: Yu surname: Zhang fullname: Zhang, Yu organization: The Key Laboratory of Molecular Epigenetics of Ministry of Education (MOE), Northeast Normal University, Changchun 130024, PR China – sequence: 10 givenname: Baiqu surname: Huang fullname: Huang, Baiqu organization: The Key Laboratory of Molecular Epigenetics of Ministry of Education (MOE), Northeast Normal University, Changchun 130024, PR China – sequence: 11 givenname: Jun surname: Lu fullname: Lu, Jun email: luj809@nenu.edu.cn organization: The Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, PR China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23583409$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1152_physiolgenomics_00024_2023 crossref_primary_10_3892_ijo_2017_4025 crossref_primary_10_1007_s10495_024_01967_0 crossref_primary_10_3390_cancers13030554 crossref_primary_10_1038_s41389_022_00397_4 crossref_primary_10_3389_fmolb_2022_928399 crossref_primary_10_3390_ijms19092838 |
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| Copyright | 2013 Crown Copyright © 2013. Published by Elsevier Inc. All rights reserved. |
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| Snippet | •Increased expression of p53 reversed the EMT phenotype.•Restoration of p53 expression suppressed EMT-mediated stem cell phenotype.•Enhanced expression of p53... Inactivation of the tumor suppressor p53 and activation of the oncogene Ras are the two most pivotal events in tumor development. However, potential... |
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| SubjectTerms | Animals Base Sequence DNA Primers EMT Epithelial-Mesenchymal Transition Flow Cytometry Fluorescent Antibody Technique Gene Silencing Genes, ras Humans Mammary Glands, Human - cytology MAP Kinase Signaling System Mice p53 Ras Stem cell Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - physiology |
| Title | p53 Attenuates the oncogenic Ras-induced epithelial–mesenchymal transition in human mammary epithelial cells |
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