miR‑106a contributes to prostate carcinoma progression through PTEN

Lu,Ji; Mu,Xupeng; Yin,Qinan; Hu,Kebang

doi:10.3892/ol.2018.9697

miR‑106a contributes to prostate carcinoma progression through PTEN

Authors:
- Ji Lu
- Xupeng Mu
- Qinan Yin
- Kebang Hu
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Affiliations: Department of Urology, The First Hospital, Jilin University, Changchun, Jilin 130021, P.R. China, Department of Central Laboratory, China‑Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China, Clinical Center, National Institute of Health, Bethesda, MD 20852, USA
Published online on: November 14, 2018 https://doi.org/10.3892/ol.2018.9697
Pages: 1327-1332

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Abstract

Prostate carcinoma is a global health problem and is estimated to be diagnosed in 1.1 million men/year, making this malignancy the second most frequently diagnosed cancer in males worldwide. micro RNAs (miRNAs) are small non‑coding RNAs that negatively regulate gene expression at the post‑transcriptional level. miRNAs contribute to cancer development and progression, and are expressed differently in normal tissues and cancers. In the present study, the biological function of miR‑106a in the human prostate carcinoma and the associated regulatory mechanisms were investigated. miR‑106a was significantly upregulated in human prostate cancer tissues when compared with normal tissues (P<0.05), and the overexpression of miR‑106a was identified to promote PC‑3 cell growth. Additionally, miRNA‑106a inhibition significantly suppressed PC‑3 cell growth. Furthermore, it was observed that the phosphatase and tensin homolog (PTEN) expression level was negatively associated with miR‑106a expression level, and miRNA‑106a directly targeted PTEN in the PC‑3 cells. PTEN overexpression has a similar effect on PC‑3 cell growth as loss of miR‑106a. Taken together, the results of the present study indicate that upregulated miR‑106a regulates PC‑3 cell proliferation through PTEN. These results suggest that appropriate manipulation of miR‑106a may provide a novel strategy in the future treatment of human prostate cancer.

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