| Issue |
E3S Web Conf.
Volume 78, 2019
2018 International Seminar on Food Safety and Environmental Engineering (FSEE 2018)
|
|
|---|---|---|
| Article Number | 01003 | |
| Number of page(s) | 4 | |
| Section | Nutrition and Health, Medical Treatment and Biomedical Engineering | |
| DOI | https://doi.org/10.1051/e3sconf/20197801003 | |
| Published online | 15 January 2019 | |
MKL1 and STAT3 activate the activity of the luciferase reporter plasmid containing the CAAP1 gene promoter
1
Henan Vocational College of Applied Technology, 450042, P.R.China.
2
Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan, 430065, PR China.
* Corresponding author: junyan8067@163.com
Breast cancer is the leading cause of cancer death in women worldwide. The etiology of the disease is not yet clear. We know that MKL1 and STAT3 play an important part in the development and progression of breast cancer. CAAP1 is a ubiquitous and highly conserved protein that is closely related to the apoptotic process of tumors. However, the definitive transcriptional mechanism of the CAAP1 gene is still unclear. In our study, we constructed a luciferase reporter plasmid for the human CAAP1 gene promoter. Then one or both of the two overexpression vectors of MKL-1 and STAT3 were co-transfected into MCF-7 cells with CAAP1 promoter plasmid, and we then tested activation of the CAAP1 promoter by luciferase reporter assay. The results show that compared with the transfected pcDNA3.1 group, MKL1 can evidently increase the transcription activity of the CAAP1 gene promoter, while the STAT3 group can slightly upregulate the transcription activity of the CAAP1 gene promoter. Our research will further reveal the relationship between CAAP1 and the occurrence and development of breast cancer cells, and provide a new idea and direction for the cures of breast cancer.
© The Authors, published by EDP Sciences, 2019
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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