| Title |
Re-expression of microRNA-4319 inhibits growth of prostate cancer via Her-2 suppression
|
|---|---|
| Published in |
Clinical and Translational Oncology, April 2018
|
| DOI | 10.1007/s12094-018-1871-y |
| Pubmed ID | |
| Authors |
X. Lin, Y. Wang |
| Abstract |
Her-2 is an epidermal growth factor receptor expressed in some prostate cancers (PC) associated with outgrowth of the tumor. Dysregulation of some microRNAs is involved in the regulation of PC pathogenesis, whereas the role of miR-4319 in PC is unknown and addressed in the current study. The levels of miR-4319 in PC tissues were determined by RT-qPCR and their association with patient survival was studied by Kaplan-Meier analysis. Targeted genes for miR-4319 were predicted by a bioinformatics algorithm and confirmed by a dual-luciferase reporter assay. Growth of cells of overexpression or inhibition of miR-4319 or Her-2 was analyzed by an MTT assay. Cell survival in response to a chemotherapeutic drug, estramustine (EM), was analyzed by CCK-8 assay. Cell apoptosis was evaluated by TUNEL assay and Western blotting for apoptosis-associated proteins. MiR-4319 levels were decreased in PC specimens, compared to corresponding normal prostate tissue. Lower levels of miR-4319 were correlated with poorer overall patients' survival. In vitro, the cell survival mediated with Her-2 against chemotherapy was inhibited by overexpression of miR-4319 and was enhanced by depletion of miR-4319. Depletion of miR-4319 in primary prostate epithelial cells increased Her-2-dependent cell growth, while re-expression of miR-4319 in PC cells inhibited Her-2-dependent cell growth and Her-2-dependent resistance to EM-induced apoptosis. The growth and chemo-resistance of PC cells may be suppressed via re-expression of miR-4319 that inhibits Her-2 signaling. |
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 % |
|---|---|---|
| Science communicators (journalists, bloggers, editors) | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 10 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 10 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 4 | 40% |
| Other | 2 | 20% |
| Student > Ph. D. Student | 1 | 10% |
| Student > Bachelor | 1 | 10% |
| Student > Master | 1 | 10% |
| Other | 0 | 0% |
| Unknown | 1 | 10% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 5 | 50% |
| Immunology and Microbiology | 1 | 10% |
| Medicine and Dentistry | 1 | 10% |
| Engineering | 1 | 10% |
| Unknown | 2 | 20% |
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 15 April 2018.
All research outputs
#18,603,172
of 23,043,346 outputs
Outputs from Clinical and Translational Oncology
#863
of 1,321 outputs
Outputs of similar age
#255,568
of 329,292 outputs
Outputs of similar age from Clinical and Translational Oncology
#21
of 29 outputs
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