| Title |
Induction of alpha-methylacyl-CoA racemase by miR-138 via up-regulation of β-catenin in prostate cancer cells
|
|---|---|
| Published in |
Journal of Cancer Research and Clinical Oncology, July 2017
|
| DOI | 10.1007/s00432-017-2484-5 |
| Pubmed ID | |
| Authors |
Kati Erdmann, Knut Kaulke, Christiane Rieger, Manfred P. Wirth, Susanne Fuessel |
| Abstract |
Alpha-methylacyl-CoA racemase (AMACR) is highly overexpressed in prostate cancer (PCa) and its transcriptional regulators include various transcription factors and CTNNB1/β-catenin. Our previous findings suggested a post-transcriptional regulation by the tumor-suppressive microRNA miR-138 in PCa. Thus, the aim of this study was to demonstrate the direct interaction of miR-138 with the 3'-UTR of AMACR. Furthermore, the influence of miR-138 on the expression of AMACR and selected AMACR regulators was investigated in PCa cells. Using DU-145, PC-3, and LNCaP PCa cells, the effect of exogenous miR-138 on AMACR and selected AMACR regulators was determined by quantitative PCR and Western blot. Luciferase reporter assays were used to verify target and promoter interaction. Using a luciferase reporter assay a direct interaction of miR-138 with the AMACR-3'-UTR was confirmed. Surprisingly, AMACR expression was up-regulated by up to 125% by exogenous miR-138 in PCa cells. The lack of any miR-138 binding sites within the AMACR promoter suggested an indirect mechanism of up-regulation. Therefore, the effect of miR-138 on selected AMACR regulators including CTNNB1/β-catenin, RELA, SMAD4, SP1, and TCF4 was evaluated. MiR-138 solely evoked an up-regulation of CTNNB1 mRNA expression and β-catenin protein levels by up to 75%. Further in silico analysis revealed a binding site for miR-138 within the CTNNB1 promoter. MiR-138 could enhance the activity of the CTNNB1 promoter, which in turn could contribute to the observed AMACR up-regulation. The present findings suggest that miR-138 can indirectly up-regulate AMACR via transcriptional induction of CTNNB1, at least in vitro in PCa cells. |
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 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 14 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 3 | 21% |
| Student > Ph. D. Student | 3 | 21% |
| Student > Bachelor | 2 | 14% |
| Student > Master | 2 | 14% |
| Professor | 1 | 7% |
| Other | 1 | 7% |
| Unknown | 2 | 14% |
| Readers by discipline | Count | As % |
|---|---|---|
| Agricultural and Biological Sciences | 4 | 29% |
| Medicine and Dentistry | 2 | 14% |
| Biochemistry, Genetics and Molecular Biology | 1 | 7% |
| Computer Science | 1 | 7% |
| Materials Science | 1 | 7% |
| Other | 0 | 0% |
| Unknown | 5 | 36% |
Attention Score in Context
This research output has an Altmetric Attention Score of 2. 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 18 October 2017.
All research outputs
#15,508,795
of 23,815,455 outputs
Outputs from Journal of Cancer Research and Clinical Oncology
#1,408
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Outputs of similar age
#190,516
of 317,686 outputs
Outputs of similar age from Journal of Cancer Research and Clinical Oncology
#19
of 39 outputs
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