MEG3 overexpression inhibits the tumorigenesis of breast cancer by downregulating miR-21 through the PI3K/Akt pathway.

Abstract

Increasing studies have highlighted the critical role of lncRNAs in cancer pathogenesis and development. LncRNA maternally expressed gene 3 (MEG3) was reported to function as a tumor suppressor in breast cancer. However, the detailed molecular mechanism of MEG3 involved in breast cancer progression remains far from being addressed. Our findings showed that MEG3 was downregulated and miR-21 was upregulated in breast cancer patient tissues and cells. MEG3 overexpression suppressed cell proliferation and glycolysis, and induced apoptosis in breast cancer cells. MEG3 was demonstrated to function as a molecular sponge of miR-21 and suppress its expression. Moreover, miR-21 upregulation partially abolished the effects of MEG3 overexpression on cell proliferation, glycolysis, and apoptosis in breast cancer cells. Additionally, enforced expression of MEG3 reversed miR-21-mediated activation of PI3K/Akt pathway in breast cancer cells. In vivo experiment demonstrated that overexpression of MEG3 inhibited tumor growth in breast cancer by suppressing miR-21. In summary, MEG3 overexpression inhibited the tumorigenesis of breast cancer by downregulating miR-21 through the PI3K/Akt pathway.

• Authors: Mingzhi Zhu, Xiaochun Wang, Yuanting Gu, Fang Wang, Lin Li, Xinguang Qiu
• Journal: Archives of biochemistry and biophysics (Arch Biochem Biophys) Vol. 661 Pg. 22-30 (01 2019) ISSN: 1096-0384 [Electronic] United States
• PMID: 30389444 (Publication Type: Journal Article)
• Copyright: Copyright © 2018 Elsevier Inc. All rights reserved.

Chemical References

• MEG3 non-coding RNA, human
• MIRN21 microRNA, human
• MicroRNAs
• RNA, Long Noncoding
• RNA, Neoplasm
• Phosphatidylinositol 3-Kinases
• Proto-Oncogene Proteins c-akt

Topics

• Animals
• Breast Neoplasms (genetics, metabolism, pathology)
• Carcinogenesis (genetics, metabolism)
• Cell Proliferation (genetics)
• Down-Regulation
• Female
• Gene Expression Regulation, Neoplastic
• Genes, Tumor Suppressor
• Humans
• MCF-7 Cells
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• MicroRNAs (biosynthesis, genetics)
• Phosphatidylinositol 3-Kinases (genetics, metabolism)
• Proto-Oncogene Proteins c-akt (genetics, metabolism)
• RNA, Long Noncoding (biosynthesis, genetics)
• RNA, Neoplasm (biosynthesis, genetics)
• Signal Transduction