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. 2019 Oct 3:12:8117-8123.
doi: 10.2147/OTT.S208133. eCollection 2019.

LncRNA LINC01116 Promotes Cancer Cell Proliferation, Migration And Invasion In Gastric Cancer By Positively Interacting With lncRNA CASC11

Xiaohui Su  1 , Jianjun Zhang  1 , Xianfeng Luo  1 , Wei Yang  1 , Yanqing Liu  1 , Yang Liu  1 , Zexing Shan  1
Affiliations

LncRNA LINC01116 Promotes Cancer Cell Proliferation, Migration And Invasion In Gastric Cancer By Positively Interacting With lncRNA CASC11

Xiaohui Su et al. Onco Targets Ther. .

Abstract

Purpose: The oncogenic roles of lncRNA LINC01116 have been reported in several types of cancer, while its involvement in gastric cancer is unknown. This study aimed to investigate the involvement of LINC01116 in gastric cancer.

Methods: Gene expression was detected by qPCR. Correlations were analyzed by linear regression. Overexpression and siRNA silencing techniques were used to analyze gene functions. Cell invasion and migration were analyzed by Transwell assays.

Results: LINC01116 and lncRNA CASC11 were both upregulated in cancer tissues compared to cancer-adjacent tissues. Expression levels of LINC01116 and CASC11 were increased with the increase in clinical stages. Expression levels of LINC01116 and CASC11 were positively correlated. Overexpression of LINC01116 mediated the upregulated CASC11 in gastric cancer cells, and CASC11 overexpression also led to overexpressed LINC01116. Overexpression of LINC01116 and CASC11 led to promoted invasion and migration of gastric cancer cells. Rescue experiments showed that CASC11 knockdown attenuated the effects of LINC01116 overexpression. Overexpression of LINC01116 failed to significantly affect cancer cell proliferation.

Conclusion: LINC01116 promoted cancer cell invasion and migration in gastric cancer by positively interacting with CASC11.

Keywords: gastric cancer; lncRNA CASC11; lncRNA LINC01116.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
LINC01116 and lncRNA CASC11 were both upregulated in gastric cancer tissues than in cancer-adjacent tissues. RT-qPCR results showed that LINC01116 (A) and CASC11 (B) were both upregulated in gastric cancer tissues than in tumor adjacent normal tissues (*p<0.05).
Figure 2
Figure 2
LINC01116 and CASC11 expression levels were increased with the increase in clinical stages. Expression levels of LINC01116 (A) and CASC11 (B) in tumor tissues were significantly increased with the increase in clinical stages (*p<0.05).
Figure 3
Figure 3
Expression levels of LINC01116 and CASC11 were positively correlated in tumor tissues and adjacent normal tissues. Linear regression showed that expression levels of LINC01116 and CASC11 were positively correlated in both tumor tissues (A) and adjacent normal tissues (B).
Figure 4
Figure 4
LINC01116 and CASC11 upregulated each other in cells of gastric cancer cell lines. Overexpression of LINC01116 and CASC11 was observed at 24h after transfection (A). Overexpression of LINC01116 mediated the upregulated CASC11 in gastric cancer cells (B), and CASC11 overexpression also led to overexpressed LINC01116 (C) (*p<0.05).
Figure 5
Figure 5
Interaction between LINC01116 and CASC11 participate in the migration and invasion of gastric cancer cells. Overexpression of LINC01116 and CASC11 led to promoted, while siRNA silencing led to suppressed migration (A) and invasion (B) of gastric cancer cells. Rescue experiments showed that CASC11 knockdown attenuated the effects of LINC01116 overexpression (*p<0.05).
See this image and copyright information in PMC

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