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. 2019 Jun;7(6):e711.
doi: 10.1002/mgg3.711. Epub 2019 May 2.

Lnc-GIHCG promotes cell proliferation and migration in gastric cancer through miR- 1281 adsorption

Guozheng Liu  1 , Zaipeng Jiang  2 , Mingliang Qiao  2 , Fengyong Wang  3
Affiliations

Lnc-GIHCG promotes cell proliferation and migration in gastric cancer through miR- 1281 adsorption

Guozheng Liu et al. Mol Genet Genomic Med. 2019 Jun.

Abstract

Background: Long noncoding RNAs (lncRNAs) are from the family of noncoding RNAs. Existing studies have shown that lncRNAs are involved in many biological processes and are strongly related to the occurrence and development of tumors. Recent studies have indicated that lncRNA GIHCG participates in the progression of many cancers by adjusting cell proliferation and migration. Gastric cancer (GC) is a prevalent malignant tumor that arises from gastric epithelium. This study mainly explored the influence of GIHCG on GC and its underlying mechanism.

Methods: GIHCG expression was detected in GC through quantitative real-time polymerase chain reaction while the relationship of GIHCG with miR-1281 and miR-1281 with TLE1 was verified using dual luciferase reporter gene assay. The influence of GIHCG, miR-1281 and TLE1 on cell function was verified using cell counting Kit-8 (CCK-8) and Transwell experiment.

Results: In GC, GIHCG was significantly overexpressed and significantly increased cell proliferation and migration, with the possible mechanism of upregulatingTLE1 expression through adsorption of miR-1281.

Conclusion: Taken together, we revealed the role of GIHCG/miR-1281/TLE1 in GC and provided a new perspective.

Keywords: GIHCG; TLE1; gastric cancer; lncRNAs; mR-1281.

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Conflict of interest statement

None declared.

Figures

Figure 1
Figure 1
Significant overexpression of GIHCG in gastric cancer. (a) Significant overexpression of GIHCG in gastric cancer tissues relative to their adjacent tissues. (b) Significantly higher expression of GIHCG in stage III‐IV patients than stage I‐II patients. (c) Survival curve analysis showing AUC of 0.8941 and a cutoff value of 0.04917. (d) Common overexpression of GIHCG in gastric cancer cell line relative to normal gastric mucosal cells. *p < 0.05, **p < 0.01, ***p < 0.001
Figure 2
Figure 2
GIHCG promoted the proliferation and migration of gastric cancer cells. (a) Significant upregulation of GIHCG expression after transfection of overexpressed plasmids of GIHCG in gastric cancer cell lines HGC‐2 and SGC‐7901. (b) Significant higher cell proliferation after upregulation of GIHCG in HGC‐27 and SGC‐7901 cells. (c) Significant higher cell migration after upregulation of GIHCG in HGC‐27 and SGC‐7901 cells. *p < 0.05, **p < 0.01, ***p < 0.001
Figure 3
Figure 3
miR‐1281 was a target gene of GIHCG. (a) Bioinformatic analysis showing their potential binding site. (b,c) Dual luciferase reporter gene assay demonstrating their binding relationship. (d) Significant lower miR‐1281 expression after upregulation of GIHCG expression in HGC‐27 and SGC‐7901 cells; E Significantly low miR‐1281 expression in gastric cancer tissues relative to adjacent tissues. (f) Negative correlation between GIHCG and miR‐1281 in gastric cancer, p < 0.05, R 2 = 0.7192. (g) After upregulation of miR‐1281 expression in HGC‐27 and SGC‐7901 cells, significant inhibition of cell proliferation and partial reversion of the promotion effect of GIHCG on cell proliferation. (h) After upregulation of miR‐1281 expression in HGC‐27 and SGC‐7901 cells, significant inhibition of cell migration and partial reversion of the promotion effect of GIHCG on cell migration. *p < 0.05, **p < 0.01, ***p < 0.001
Figure 4
Figure 4
TLE1 was a potential target gene of miR‐1281. (a) Bioinformatic analysis showing their potential binding site. (b,c) Dual luciferase reporter gene assay showing their binding relationship. (d,e) Significant lower TLE1 expression at protein and mRNA levels after upregulation of miR‐1281 expression in HGC‐27 and SGC‐7901 cells. *p < 0.05, **p < 0.01, ***p < 0.001
Figure 5
Figure 5
miR‐1281 exerted its role through downregulation of TLE1. (a) Significantly higher TLE1 expression in gastric cancer tissues than in their adjacent tissues. (b) TLE1 negatively correlated with miR‐1281 in gastric cancer, p < 0.05, R 2 = 0.4552. (c,d) After upregulation of TLE1 expression in HGC‐27 and SGC‐7901 cells, significantly higher cell proliferation and partial reversion of the suppression of miR‐1281 on cell proliferation. (e) After upregulation of TLE1 expression in SGC‐7901 and HGC‐27 cells, significantly higher cell migration and partial reversion of the suppression of miR‐1281 on cell migration. *p < 0.05, **p < 0.01, ***p < 0.001
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