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In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium

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In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium. / Latonen, Leena; Scaravilli, Mauro; Gillen, Andrew; Hartikainen, Samuli; Zhang, Fu Ping; Ruusuvuori, Pekka; Kujala, Paula; Poutanen, Matti; Visakorpi, Tapio.

In: American Journal of Pathology, Vol. 187, No. 11, 01.11.2017, p. 2546-2557.

Research output: Contribution to journalArticleScientificpeer-review

Harvard

Latonen, L, Scaravilli, M, Gillen, A, Hartikainen, S, Zhang, FP, Ruusuvuori, P, Kujala, P, Poutanen, M & Visakorpi, T 2017, 'In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium', American Journal of Pathology, vol. 187, no. 11, pp. 2546-2557. https://doi.org/10.1016/j.ajpath.2017.07.012

APA

Latonen, L., Scaravilli, M., Gillen, A., Hartikainen, S., Zhang, F. P., Ruusuvuori, P., ... Visakorpi, T. (2017). In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium. American Journal of Pathology, 187(11), 2546-2557. https://doi.org/10.1016/j.ajpath.2017.07.012

Vancouver

Latonen L, Scaravilli M, Gillen A, Hartikainen S, Zhang FP, Ruusuvuori P et al. In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium. American Journal of Pathology. 2017 Nov 1;187(11):2546-2557. https://doi.org/10.1016/j.ajpath.2017.07.012

Author

Latonen, Leena ; Scaravilli, Mauro ; Gillen, Andrew ; Hartikainen, Samuli ; Zhang, Fu Ping ; Ruusuvuori, Pekka ; Kujala, Paula ; Poutanen, Matti ; Visakorpi, Tapio. / In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium. In: American Journal of Pathology. 2017 ; Vol. 187, No. 11. pp. 2546-2557.

Bibtex - Download

@article{255e6dd2712c4cd2920d36cdadd8c14f,
title = "In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium",
abstract = "miRNAs are important regulators of gene expression and are often deregulated in cancer. We have previously shown that miR-32 is an androgen receptor–regulated miRNA overexpressed in castration-resistant prostate cancer and that miR-32 can improve prostate cancer cell growth in vitro. To assess the effects of miR-32 in vivo, we developed transgenic mice overexpressing miR-32 in the prostate. The study indicated that transgenic miR-32 expression increases replicative activity in the prostate epithelium. We further observed an aging-associated increase in the incidence of goblet cell metaplasia in the prostate epithelium. Furthermore, aged miR-32 transgenic mice exhibited metaplasia-associated prostatic intraepithelial neoplasia at a low frequency. When crossbred with mice lacking the other allele of tumor-suppressor Pten (miR-32xPten+/− mice), miR-32 expression increased both the incidence and the replicative activity of prostatic intraepithelial neoplasia lesions in the dorsal prostate. The miR-32xPten+/− mice also demonstrated increased goblet cell metaplasia compared with Pten+/− mice. By performing a microarray analysis of mouse prostate tissue to screen downstream targets and effectors of miR-32, we identified RAC2 as a potential, and clinically relevant, target of miR-32. We also demonstrate down-regulation of several interesting, potentially prostate cancer–relevant genes (Spink1, Spink5, and Casp1) by miR-32 in the prostate tissue. The results demonstrate that miR-32 increases proliferation and promotes metaplastic transformation in mouse prostate epithelium, which may promote neoplastic alterations in the prostate.",
author = "Leena Latonen and Mauro Scaravilli and Andrew Gillen and Samuli Hartikainen and Zhang, {Fu Ping} and Pekka Ruusuvuori and Paula Kujala and Matti Poutanen and Tapio Visakorpi",
year = "2017",
month = "11",
day = "1",
doi = "10.1016/j.ajpath.2017.07.012",
language = "English",
volume = "187",
pages = "2546--2557",
journal = "American Journal of Pathology",
issn = "0002-9440",
publisher = "American Society for Investigative Pathology",
number = "11",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - In Vivo Expression of miR-32 Induces Proliferation in Prostate Epithelium

AU - Latonen, Leena

AU - Scaravilli, Mauro

AU - Gillen, Andrew

AU - Hartikainen, Samuli

AU - Zhang, Fu Ping

AU - Ruusuvuori, Pekka

AU - Kujala, Paula

AU - Poutanen, Matti

AU - Visakorpi, Tapio

PY - 2017/11/1

Y1 - 2017/11/1

N2 - miRNAs are important regulators of gene expression and are often deregulated in cancer. We have previously shown that miR-32 is an androgen receptor–regulated miRNA overexpressed in castration-resistant prostate cancer and that miR-32 can improve prostate cancer cell growth in vitro. To assess the effects of miR-32 in vivo, we developed transgenic mice overexpressing miR-32 in the prostate. The study indicated that transgenic miR-32 expression increases replicative activity in the prostate epithelium. We further observed an aging-associated increase in the incidence of goblet cell metaplasia in the prostate epithelium. Furthermore, aged miR-32 transgenic mice exhibited metaplasia-associated prostatic intraepithelial neoplasia at a low frequency. When crossbred with mice lacking the other allele of tumor-suppressor Pten (miR-32xPten+/− mice), miR-32 expression increased both the incidence and the replicative activity of prostatic intraepithelial neoplasia lesions in the dorsal prostate. The miR-32xPten+/− mice also demonstrated increased goblet cell metaplasia compared with Pten+/− mice. By performing a microarray analysis of mouse prostate tissue to screen downstream targets and effectors of miR-32, we identified RAC2 as a potential, and clinically relevant, target of miR-32. We also demonstrate down-regulation of several interesting, potentially prostate cancer–relevant genes (Spink1, Spink5, and Casp1) by miR-32 in the prostate tissue. The results demonstrate that miR-32 increases proliferation and promotes metaplastic transformation in mouse prostate epithelium, which may promote neoplastic alterations in the prostate.

AB - miRNAs are important regulators of gene expression and are often deregulated in cancer. We have previously shown that miR-32 is an androgen receptor–regulated miRNA overexpressed in castration-resistant prostate cancer and that miR-32 can improve prostate cancer cell growth in vitro. To assess the effects of miR-32 in vivo, we developed transgenic mice overexpressing miR-32 in the prostate. The study indicated that transgenic miR-32 expression increases replicative activity in the prostate epithelium. We further observed an aging-associated increase in the incidence of goblet cell metaplasia in the prostate epithelium. Furthermore, aged miR-32 transgenic mice exhibited metaplasia-associated prostatic intraepithelial neoplasia at a low frequency. When crossbred with mice lacking the other allele of tumor-suppressor Pten (miR-32xPten+/− mice), miR-32 expression increased both the incidence and the replicative activity of prostatic intraepithelial neoplasia lesions in the dorsal prostate. The miR-32xPten+/− mice also demonstrated increased goblet cell metaplasia compared with Pten+/− mice. By performing a microarray analysis of mouse prostate tissue to screen downstream targets and effectors of miR-32, we identified RAC2 as a potential, and clinically relevant, target of miR-32. We also demonstrate down-regulation of several interesting, potentially prostate cancer–relevant genes (Spink1, Spink5, and Casp1) by miR-32 in the prostate tissue. The results demonstrate that miR-32 increases proliferation and promotes metaplastic transformation in mouse prostate epithelium, which may promote neoplastic alterations in the prostate.

U2 - 10.1016/j.ajpath.2017.07.012

DO - 10.1016/j.ajpath.2017.07.012

M3 - Article

VL - 187

SP - 2546

EP - 2557

JO - American Journal of Pathology

JF - American Journal of Pathology

SN - 0002-9440

IS - 11

ER -