Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α
Received 10 November 2019
Accepted for publication 20 February 2020
Published 27 March 2020 Volume 2020:12 Pages 2301—2314
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Ahmet Emre Eskazan
Xuefeng Jiang,1,* Yusheng Liu,1,* Guijuan Zhang,2,* Shujun Lin,1 Naijun Yuan,1 Jieyan Wu,1 Xianxin Yan,1 Yi Ma,3 Min Ma1,2
1College of Traditional Chinese Medicine of Jinan University, Guangzhou, People’s Republic of China; 2The First Affiliated Hospital of Jinan University, Guangzhou, People’s Republic of China; 3Institute of Biomedicine and Department of Cellular Biology, Jinan University, Guangzhou, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Min Ma
College of Traditional Chinese Medicine of Jinan University, 601 Huangpu Avenue West, Guangzhou, Guangdong 510632, People’s Republic of China
Tel +86 15876583624
Fax +86 20-85227173
Purpose: Acetyl-11-keto-β-boswellic acid (AKBA) has therapeutic effects on a range of diseases, including tumours. lncRNAs, as competing endogenous RNAs (ceRNAs), can interact with miRNAs to regulate the expression of target genes, which can affect the development of tumors. Here, we examined the effects of AKBA on breast precancerous lesions MCF-10AT cells.
Methods: The expression profiles of breast cancer (BC) tissue were collated from The Cancer Genome Atlas (TCGA), and the lncRNA-miRNA-mRNA ceRNA network was constructed. AKBA targets were predicted by network pharmacology. The expression of long intergenic nonprotein-coding RNA 707 (LINC00707), miR-206 and ER-α was determined by qRT-PCR. Cell viability, apoptosis and cycle were assessed by CCK-8 and flow cytometry. Protein levels were measured by Western blotting.
Results: A total of 3205 differentially expressed mRNAs, 104 miRNAs, and 605 lncRNAs were identified. The ceRNA network consisting of 9 lncRNAs, 15 miRNAs and 82 mRNAs was constructed. We found that LINC00707 was up-regulated and miR-206 was down-regulated in MCF-10AT cells. Transfected si-LINC00707 could inhibit cell proliferation, induce cell apoptosis and cycle arrest of MCF-10AT cells. In addition, network pharmacology predicted that AKBA may regulate the ESR1 in the treatment of BC. Our research demonstrated that AKBA could induce cell apoptosis and G1-phase arrest and inhibit ER-α expression via LINC00707/miR-206 in MCF-10AT cells.
Conclusion: AKBA inhibited MCF-10AT cells via regulation of LINC00707/miR-206 that reduces ER-α.
Keywords: breast precancerous lesion, acetyl-11-keto-β-boswellic acid, ceRNA, LINC00707, miR-206, ESR1
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