Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α

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, Peo...

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Main Authors: Jiang X, Liu Y, Zhang G, Lin S, Yuan N, Wu J, Yan X, Ma Y, Ma M
Format: Article
Language:English
Published: Dove Medical Press 2020-03-01
Series:Cancer Management and Research
Subjects:
Online Access:https://www.dovepress.com/acetyl-11-keto-beta-boswellic-acid-inhibits-precancerous-breast-lesion-peer-reviewed-article-CMAR
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author Jiang X
Liu Y
Zhang G
Lin S
Yuan N
Wu J
Yan X
Ma Y
Ma M
author_facet Jiang X
Liu Y
Zhang G
Lin S
Yuan N
Wu J
Yan X
Ma Y
Ma M
author_sort Jiang X
collection DOAJ
description 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 workCorrespondence: Min MaCollege of Traditional Chinese Medicine of Jinan University, 601 Huangpu Avenue West, Guangzhou, Guangdong 510632, People’s Republic of ChinaTel +86 15876583624Fax +86 20-85227173Email 2246809300@qq.comPurpose: 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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spelling doaj.art-612132ecdd944cc6800a915566710e012022-12-21T20:32:00ZengDove Medical PressCancer Management and Research1179-13222020-03-01Volume 122301231452759Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-αJiang XLiu YZhang GLin SYuan NWu JYan XMa YMa MXuefeng 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 workCorrespondence: Min MaCollege of Traditional Chinese Medicine of Jinan University, 601 Huangpu Avenue West, Guangzhou, Guangdong 510632, People’s Republic of ChinaTel +86 15876583624Fax +86 20-85227173Email 2246809300@qq.comPurpose: 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, ESR1https://www.dovepress.com/acetyl-11-keto-beta-boswellic-acid-inhibits-precancerous-breast-lesion-peer-reviewed-article-CMARbreast precancerous lesionacetyl-11-keto-β-boswellic acidcernalinc00707mir-206esr1
spellingShingle Jiang X
Liu Y
Zhang G
Lin S
Yuan N
Wu J
Yan X
Ma Y
Ma M
Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α
Cancer Management and Research
breast precancerous lesion
acetyl-11-keto-β-boswellic acid
cerna
linc00707
mir-206
esr1
title Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α
title_full Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α
title_fullStr Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α
title_full_unstemmed Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α
title_short Acetyl-11-keto-β-boswellic Acid Inhibits Precancerous Breast Lesion MCF-10AT Cells via Regulation of LINC00707/miR-206 that Reduces Estrogen Receptor-α
title_sort acetyl 11 keto beta boswellic acid inhibits precancerous breast lesion mcf 10at cells via regulation of linc00707 mir 206 that reduces estrogen receptor alpha
topic breast precancerous lesion
acetyl-11-keto-β-boswellic acid
cerna
linc00707
mir-206
esr1
url https://www.dovepress.com/acetyl-11-keto-beta-boswellic-acid-inhibits-precancerous-breast-lesion-peer-reviewed-article-CMAR
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