lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184

Xie,Qiang; Zhao,Shankun; Kang,Ran; Wang,Xiaolan

doi:10.3892/ijmm.2021.5015

lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184

Authors:
- Qiang Xie
- Shankun Zhao
- Ran Kang
- Xiaolan Wang
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Affiliations: Department of Reproduction, Affiliated Dongguan Hospital, Southern Medical University, Dongguan, Guangdong 523059, P.R. China, Department of Urology, Taizhou Central Hospital (Taizhou University Hospital), Zhejiang, Taizhou 318000, P.R. China, Department of Urology, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China, Reproductive Center of Medicine, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China
Published online on: July 28, 2021 https://doi.org/10.3892/ijmm.2021.5015
Article Number: 182
Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Long non‑coding RNA (lncRNA) small nucleolar RNA host gene 11 (SNHG11) has been shown to play an important role in the development and progression of numerous types of cancer. However, to the best of our knowledge, the role of SNHG11 in prostate cancer (PCa) development and metastasis remains unclear. Thus, the aim of the present study was to investigate the functional role and molecular mechanisms of SNHG11 in PCa progression. It was revealed that the SNHG11 expression levels were significantly upregulated in PCa tissues, in comparison with those in adjacent normal tissues. Functionally, SNHG11 knockdown significantly suppressed PCa cell proliferation, migration, invasion and metastasis in vitro and in vivo. Furthermore, SNHG11 was found to positively regulate insulin‑like growth factor 1 receptor (IGF‑1R) expression by sponging microRNA (miRNA/miR)‑184 in PCa cells. The results of rescue experiments demonstrated that IGF‑1R overexpression reversed the suppressive effects of SNHG11 knockdown on the proliferation, migration and invasion of PCa cells. On the whole, the findings of the present study suggest that SNHG11 expression is upregulated in PCa and that it facilitates PCa progression, at least in part, via the modulation of the miR‑184/IGF‑1R signaling axis.

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