miR-29 family inhibited the proliferation and migration of lung cancer cells by targeting SREBP-1.

Autor: Lin, Lin, Bao, Yongxia, Tian, Miao, Ren, Qiu, Zhang, Wei
Zdroj: Molecular & Cellular Toxicology; Apr2022, Vol. 18 Issue 2, p165-175, 11p
Abstrakt: Backgrounds: Lipid metabolism dysregulation is an important characteristic of tumor cells. Increased lipid metabolism provides a vital material and energy source for tumor growth, thereby promoting tumor invasion and metastasis. Objectives: In the current work, we carried out a series of in vivo and in vitro studies to explore the relationship between miR-29 and lung cancer. Results: The results showed that miR-29 was down-regulated in lung cancer, and overexpression of miR-29 inhibited the proliferation and migration of lung cancer cells (in vitro). Anti-lung cancer effect of miR-29 in vivo was evaluated, and results indicated that transfection of miR-29b/c markedly inhibited lung tumor growth (in vivo). We further explored the potential mechanism by which miR-29 could inhibit the cell proliferation of lung cancer. It is well known that lipid metabolism dysregulation is an important characteristic of tumor cells. Increased lipid metabolism provides a vital material and energy source for tumor growth, thereby promoting tumor invasion and metastasis, and sterol regulatory element-binding protein 1 (SREBP) is involved in liposome metabolism. Therefore, we analyzed the interaction between miR-29C and SREBP-1 in lung cancer cells. Bioinformatics analysis showed that the miR-29 has the potential binding site on SCAP and SREBP mRNA, and Luciferase reporter gene assays revealed the interaction between 3′UTR of SREBP-1 mRNA and miR-29c. Further study showed that miR-29 suppressed (SREBP-1) expression by interacting with 3′UTR of SREBP-1. Further work indicated that miR-29 transfection strongly inhibited lung cancer cell proliferation, which was rescued by the overexpression of SREBP-1. Conclusion: These findings demonstrate that transfection of miR-29 suppressed lung cancer proliferation via inhibiting SREBP-1 expression. The current study provides a basis for exploring the targeted agents against lung cancer. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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