MicroRNA-30a-5p inhibits the proliferation and invasion of gastric cancer cells by targeting insulin-like growth factor 1 receptor
Authors: Yang Liu
Changjie Zhang
Yu Zhou
Xun Gong
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: gastric cancer; insulin-like growth factor 1 receptor; invasion; microRNA-30a-5p; proliferation.
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.

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&lt;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&lt;0.01). In addition, overexpression of miR-30a-5p significantly inhibited the proliferation and invasion of AGS cells (P&lt;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&lt;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&lt;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&lt;0.01), and its levels of expression were reversely correlated with that of miR-30a-5p in gastric cancer tissues (R2=0.3892; P&lt;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. 

Retracted: Yes

PubPeer comments:
 Supplemental Fig. 1C: Blot doesn t match with the raw data. Could authors check please? ![file] , 
 #1 lower band under the red dotted line? , 
 #1 It looks like it does fit, but the red frame is misplaced. The right band appears to be just 1 cm lower, partially covered by the bottom part of the frame. Although one wonders, which one is the right band? Needs clarification anyway. , 
 We apologize for this mistake that occurred in figure preparation. There are basically two issues identified here: 1. During figure preparation the red rectangle in the data source to indicate the cropped image moved up and selected a non-specific band that was above the signal of the phosphorylated form of eIF2u03b1. We didn t notice this despite having a clear positive control with Tunicamycin treatment (Figure 1A). 2. When we assembled the final figure the areas did not match to all panels, and to maintain the symmetry of the figure the image was enlarged in the height (instead of rescanning the original film to include a larger area). We apologize for this practice of stretching this band, but as you can conclude the figure matches with the raw data provided. A correction at the journal has been filed and accepted (see email exchange in data repository at www.hetzlab.cl data) to replace the supplementary information at Nature Communications with a corrected version (Figure 1B-C). We apologize for this mistake in figure preparation. Importantly, the biological conclusion of the experiment is not altered by this mistake. ![file] **Figure 1. Raw data presentation and figure correction.** (A) Band selection of the raw data blot of the phosphorylated form of eIF2u03b1 in the old version of the manuscript submitted to Nature Communications Journal. (B) Corrected band selection of the raw data blot. This selection includes two bands where the lower one corresponds to the specific signal of the antibody. (C) Corrected supplementary figure 1 submitted and accepted as correction in Nature Communications (*, unspecific band, the arrow indicates the specific band for P-eIF2u03b1). , 
 In the corrected Supp Figure 1c, how do the authors know which band is P-e1F2alpha? Why does the antibody they used react more strongly with non-specific band than with P-e1F2alpha? Which antibody was used? Have other investigators found that it binds to another protein of similar molecular mass to e1F2alpha? ,