Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster display

1533 - Syndecan-1 up-regulates microRNA-331-3p and mediates epithelial-to-mesenchymal transition in prostate cancer

Date

10 Oct 2016

Session

Poster display

Presenters

Tomomi Fujii

Citation

Annals of Oncology (2016) 27 (6): 545-551. 10.1093/annonc/mdw393

Authors

T. Fujii1, K. Shimada1, Y. Tatsumi1, N. Tanaka2, K. Fujimoto3, N. Konishi1

Author affiliations

  • 1 Pathology, Nara Medical University, 634-8521 - Nara/JP
  • 2 Urology, Nara Medical University Hospital, 634-8522 - Kashihara/JP
  • 3 Urology, Nara Medical University Hospital, Kashihara/JP
More

Resources

Abstract 1533

Background

Syndecan-1 is an important regulator, and may contribute to various mechanisms in the progression of prostate cancer, such as cell growth, and epithelial-to-mesenchymal transition (EMT), through regulation of microRNAs (miRNAs). We recently found that miR-331-3p is down-regulated by syndecan-1 silencing in PC3 cells, based on an miRNA expression array and quantitative RT-PCR assay. The aim of the present study was to investigate whether syndecan-1-regulated miR-331-3p expression positively affects EMT.

Methods

The expression of miR-331-3p, E-cadherin, and vimentin was detected in twenty-three prostate cancer tissues with in situ hybridization and immunohistochemistry. For functional analysis of miR-331-3p and syndecan-1, miR-331-3p precursor or syndecan-1 siRNA was transfected into PC3 cell lines. Cell proliferation and migration were evaluated with MTS assay and wound healing assay, respectively. For bioinformatics prediction, quantitative RT-PCR and luciferase assay were used to identify the target of the miRNA.

Results

In situ hybridization and immunohistochemistry of radical prostatectomy samples revealed miR-331-3p expression in cancer cells with high Gleason patterns, and EMT was demonstrated by decreased E-cadherin and increased vimentin staining. Overexpression of miR-331-3p up-regulated mesenchymal markers such as vimentin, N-cadherin, and Snail, and down-regulated epithelial markers such as E-cadherin and desmoplakin in the prostate cancer cell line PC3. We identified Neuropilin 2 (NRP2) and nucleus accumbens-associated protein 1 (NACC1) as putative target molecules in silico, as they were closely associated with the expression of miR-331-3p and TGF-ß/Smad 4 signals. Syndecan-1 gene silencing decreased the levels of Dicer, which is involved in miRNA maturation.

Conclusions

miR-331-3p can suppress tumor growth and the migration of prostate cancer cells by targeting NRP2 and NACC1, which may provide a potential therapeutic target for prostate cancer treatment. Moreover, syndecan-1-mediated miRNA maturation by Dicer and miR-331-3p-mediated EMT via effects on TGF-ß/Smad 4 signaling are essential for the development of prostate cancer.

Clinical trial identification

Legal entity responsible for the study

Nara Medical University School of Medicine, Nara, Japan

Funding

Grant-in-Aid from the Ministry of Educaion, Culture, Sports, Science and Technology, Japan (26462424)

Disclosure

All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings