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lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF‑1R expression and by sponging miR‑184
Author(s) -
Qiang Xie,
Shankun Zhao,
Ran Kang,
Xiaolan Wang
Publication year - 2021
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2021.5015
Subject(s) - gene knockdown , downregulation and upregulation , cancer research , oncogene , biology , prostate cancer , long non coding rna , microrna , metastasis , cell growth , cell cycle , cancer , tumor progression , apoptosis , gene , genetics
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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