MicroRNA‑30a‑5p inhibits the proliferation and invasion of gastric cancer cells by targeting insulin‑like growth factor 1 receptor Retraction in /10.3892/etm.2021.10728

Liu,Yang; Zhou,Yu; Gong,Xun; Zhang,Changjie

doi:10.3892/etm.2017.4477

MicroRNA‑30a‑5p inhibits the proliferation and invasion of gastric cancer cells by targeting insulin‑like growth factor 1 receptor

Retraction in: /10.3892/etm.2021.10728

Authors:
- Yang Liu
- Yu Zhou
- Xun Gong
- Changjie Zhang
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Affiliations: Department of Rehabilitation, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China, Department of Neurosurgery, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China, Department of Emergency, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China
Published online on: May 18, 2017 https://doi.org/10.3892/etm.2017.4477
Pages: 173-180
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNAs (miRs) are a class of small non-coding RNAs of 18-25 nucleotides in length that serve as key regulators in the development and progression of human cancers. Recently, miR‑30b‑5p, as a member of the miR‑30 family, has been reported to act as a tumor suppressor in gastric cancer. However, the expression and function of miR‑30a‑5p in gastric cancer, as well as the corresponding underlying mechanism, remain unknown. In the present study, it was demonstrated that the expression of miR‑30a‑5p was significantly reduced in gastric cancer tissues (n=43) compared with normal gastric tissues (n=10; P<0.01). Similarly, miR‑30a‑5p was significantly downregulated in the gastric cancer cell lines AGS, HGC27, BGC823 and SGC7901, when compared with the normal gastric mucosa epithelial cell line GES‑1 (P<0.01). In addition, overexpression of miR‑30a‑5p significantly inhibited the proliferation and invasion of AGS cells (P<0.01). Insulin‑like growth factor 1 receptor (IGF‑1R) was identified as a novel target of miR‑30a‑5p, and the protein expression of IGF‑1R was negatively regulated by miR‑30a‑5p in AGS cells (P<0.01). Furthermore, overexpression of IGF‑1R significantly reversed the inhibitory effect of miR‑30a‑5p on the proliferation and invasion of AGS cells (P<0.01), indicating that IGF‑1R was involved in miR‑30a‑5p‑mediated proliferation and invasion of AGS cells. It was also observed that the expression of IGF‑1R mRNA was upregulated in gastric cancer tissues compared with normal gastric tissues (P<0.01), and its levels of expression were reversely correlated with that of miR‑30a‑5p in gastric cancer tissues (R2=0.3892; P<0.01). Collectively, these data suggest that miR‑30a‑5p inhibits the growth and metastasis of gastric cancer by directly targeting IGF‑1R. Therefore, the miR‑30a‑5p/IGF‑1R axis may be a potential therapeutic target in the treatment of gastric cancer.

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