Evidence map›Paper›PMID 40029493›Full record

ArticleBreast cancer (Tokyo, Japan)2025

c-Myc knockdown restores tamoxifen sensitivity in triple-negative breast cancer by reactivating the expression of ERα: the central role of miR-152 and miR-148a.

Chao Dong, Yonghong Sun, Xiaoli Xu, Huiling Li, Xinyu Song, Wenxin Wei, Chong Jiao, Haoyi Xu, Yuanjing Liu, Zuliyaer Mierzhakenmu and 2 more

Abstract read
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Article in Breast cancer (Tokyo, Japan), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Exploring the therapeutic potential andFrontiers in pharmacology · 2025
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

12 authors.

Chao DongDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Yonghong SunDepartment of Central Operating Room, The Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Xiaoli XuDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Huiling LiDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Xinyu SongDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Wenxin WeiDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Chong JiaoDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Haoyi XuDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Yuanjing LiuDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Zuliyaer MierzhakenmuDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Li LiDepartment of Gynecological Oncology (First Ward), The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China. 15699212127@163.com.
Binlin MaDepartment of Breast and Thyroid Surgery, the Clinical Medical Research Center of Breast and Thyroid Tumor in Xinjiang, The Affiliated Tumor Hospital of Xinjiang Medical University, No. 789 Suzhou East Street, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China. 18099193595@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPoor prognosis of triple-negative breast cancer (TNBC) is owing to its intrinsic heterogeneity and lack of targeted therapies. Emerging evidence has characterized that targeting c-Myc might be a promising way to treat TNBC.

methodsc-Myc knocked down TNBC cells were generated and the tamoxifen sensitivity was determined. Methylation-specific PCR analysis was used to detect the methylation status of ERα promoter, and c-Myc-mediated miRNA transcription was examined using chromatin immunoprecipitation and dual-luciferase reporter assays. The in vivo tamoxifen sensitivity was determined by mouse xenograft model.

resultsc-Myc knockdown in TNBC cells leads to the reactivation of ERα and consequent acquisition its sensitivity to tamoxifen. c-Myc depletion decreased the methylation in the promoter of ERα and DNMT1 was identified as the main executor. c-Myc knockdown-induced tamoxifen sensitivity was reversed by DNMT1 overexpression. The expression of miR-152-3p and miR-148a-3p was largely induced in c-Myc knockdown TNBC cells, and both miR-152-3p and miR-148a-3p could target DNMT1 to regulate its expression. c-Myc binds to the promoter regions of miR-152-3p and miR-148a-3p to exert transcriptional suppression. By suppressing miR-152-3p or miR-148a-3p expression using inhibitors, enhanced sensitivity to tamoxifen induced by c-Myc knockdown was partially reversed. In vivo xenograft tumor model demonstrated that c-Myc knockdown mildly inhibits the growth of tumor, and a dramatic decline was observed when administrated with tamoxifen combined with c-Myc knockdown.

conclusionOur study first illustrated that c-Myc knockdown in TNBC cells reactivate ERα expression in a miR-152/miR-148a-DNMT1-dependent manner, and brought new sights into treating TNBC using hormonal therapies.

Indexed as

Drug Resistance, NeoplasmEstrogen Receptor alphaMicroRNAsProto-Oncogene Proteins c-mycTamoxifenTriple Negative Breast NeoplasmsAnimalsAntineoplastic Agents, HormonalCell Line, TumorDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMiceAntineoplastic Agents, HormonalDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanESR1 protein, humanEstrogen Receptor alphaMicroRNAsMIRN148 microRNA, humanMIRN152 microRNA, humanMYC protein, humanProto-Oncogene Proteins c-mycTamoxifenc-MycDNMT1miR-152 and miR-148aTamoxifen sensitivityTranscriptional regulationTriple-negative breast cancer

Identifiers

PMID40029493

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