LINC01133 Hampers the Development of Gastric Cancer Through Increasing Somatostatin via Binding to microRNA-576-5p

Abstract

Aim: Our study aimed at investigating how LINC01133 functions in gastric cancer (GC) progression. Materials & methods: Gain-of-function and loss-of-function approaches were applied to analyze the effects of LINC01133, microRNA-576-5p (miR-576-5p) and somatostatin (SST) on the biological behaviors of GC cells and in tumor-bearing nude mice. Results: GC tissues and cells showed low expression of LINC01133, and LINC01133 overexpression decreased malignant phenotypes of GC cells. Moreover, LINC01133 upregulated SST through binding to miR-576-5p. Overexpressing miR-576-5p or suppressing SST reversed the functions of LINC01133 in biological potentials of GC cells and tumor growth. Conclusion: LINC01133 overexpression may inhibit GC development by downregulation of miR-576-5p and upregulation of SST, which suggests new therapeutic targets for GC.

Keywords::

• apoptosis
• gastric cancer
• invasion
• LINC01133
• microRNA-576-5p
• migration
• progression
• proliferation
• SST
• therapy

Acknowledgments

The authors would like to thank all participants that enrolled in the present study.

Financial & competing interests disclosure

This work was supported by the National Key R & D Program of China (number 2019YFE0190500); study on the mechanism of MiR-3188 targeting mTOR signaling in the regulation of Imatinib in gastrointestinal stromal tumors (number 2016JC2048); establishment and application of comprehensive intervention demonstration system for hereditary tumors (number 2017SK103); the Natural Science Foundation of China Hunan Science & Technology Department (number 2019JJ40429) and Science and Health Joint Project of Natural Science Foundation of Hunan Province (number 2018JJ6048). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations. In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.

Data sharing statement

The datasets generated/analyzed during the current study are available.

Additional information

Funding

This work was supported by the National Key R & D Program of China (number 2019YFE0190500); study on the mechanism of MiR-3188 targeting mTOR signaling in the regulation of Imatinib in gastrointestinal stromal tumors (number 2016JC2048); establishment and application of comprehensive intervention demonstration system for hereditary tumors (number 2017SK103); the Natural Science Foundation of China Hunan Science & Technology Department (number 2019JJ40429) and Science and Health Joint Project of Natural Science Foundation of Hunan Province (number 2018JJ6048). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.