| Title |
PTEN insufficiency modulates ER+ breast cancer cell cycle progression and increases cell growth in vitro and in vivo
|
|---|---|
| Published in |
Drug Design, Development and Therapy, August 2015
|
| DOI | 10.2147/dddt.s86184 |
| Pubmed ID | |
| Authors |
Kun-Chun Chiang, Huang-Yang Chen, Shu-Yuan Hsu, Jong-Hwei S Pang, Shang-Yu Wang, Jun-Te Hsu, Ta-Sen Yeh, Li-Wei Chen, Sheng-Fong Kuo, Chi-Chin Sun, Jim-Ming Lee, Chun-Nan Yeh, Horng-Heng Juang |
| Abstract |
Phosphatase and tensin homolog (PTEN), a well-known tumor suppressor gene and frequently mutated or lost in breast cancer, possesses the negative regulation function over the PI3K/Akt/mTOR pathway. PTEN insufficiency has been associated with advanced breast cancer and poor prognosis of breast cancer patients. Recently, target therapies aimed at PI3K/Akt/mTOR pathway to treat breast cancer have got popularity. However, the exact effect of PTEN on breast cancer cells is still not well understood. This study demonstrated that PTEN knockdown in MCF-7 cells strengthened the downstream gene expressions, including p-Akt, p-ERK1/2, p-mTOR, p-p70s6k, and p-GSK3β. PTEN knockdown MCF-7 cells had increased cell growth and Ki-67 expression. Further Western blot demonstrated that p27 was repressed obviously with p21 slightly inhibited and CDK1, 2, 4, 6, cyclin A, and Cdc25C were upregulated in MCF-7 PTEN knockdown cells, leading to the higher growth rate. More importantly, PTEN knockdown MCF-7 cells had higher tumorigenesis and tumor growth in vivo. From our current work, we provided more detailed PTEN-mediated mechanisms to stimulate ER+ breast cancer cell growth. Our result may pave the way for further target therapy development used alone or in combination with other drugs for ER+ breast cancer with PTEN insufficiency. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Practitioners (doctors, other healthcare professionals) | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 25 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 25 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 6 | 24% |
| Student > Ph. D. Student | 4 | 16% |
| Student > Master | 3 | 12% |
| Researcher | 2 | 8% |
| Professor | 2 | 8% |
| Other | 4 | 16% |
| Unknown | 4 | 16% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 7 | 28% |
| Agricultural and Biological Sciences | 5 | 20% |
| Medicine and Dentistry | 3 | 12% |
| Immunology and Microbiology | 1 | 4% |
| Neuroscience | 1 | 4% |
| Other | 0 | 0% |
| Unknown | 8 | 32% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 August 2015.
All research outputs
#20,655,488
of 25,371,288 outputs
Outputs from Drug Design, Development and Therapy
#1,437
of 2,268 outputs
Outputs of similar age
#202,328
of 276,419 outputs
Outputs of similar age from Drug Design, Development and Therapy
#100
of 151 outputs
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