Evidence map›Paper›PMID 22074923›Full record

ArticleThe Journal of biological chemistry2012

MicroRNA 34c gene down-regulation via DNA methylation promotes self-renewal and epithelial-mesenchymal transition in breast tumor-initiating cells.

Fengyan Yu, Yu Jiao, Yinghua Zhu, Ying Wang, Jingde Zhu, Xiuying Cui, Yujie Liu, Yinghua He, Eun-Young Park, Hongyu Zhang and 5 more

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed.

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  13. MicroRNA Regulation of Breast Cancer Stemness.International journal of molecular sciences · 2021
    Review
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Fengyan YuDepartment of Breast Surgery, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China.
Yu JiaoSchool of Life Sciences, Sun-Yat-Sen University, Guangzhou 510006, China.
Yinghua ZhuSchool of Life Sciences, Sun-Yat-Sen University, Guangzhou 510006, China.
Ying WangDepartment of Breast Surgery, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China.
Jingde ZhuCancer Epigenetics and Gene Therapy Group, Shanghai Cancer Institute, Shanghai Jiaotong University, Shanghai 200032, China.
Xiuying CuiCenter of Medical Research, Sun Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China.
Yujie LiuDepartment of Breast Surgery, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China.
Yinghua HeCancer Epigenetics and Gene Therapy Group, Shanghai Cancer Institute, Shanghai Jiaotong University, Shanghai 200032, China.
Eun-Young ParkDepartment of Biological Science, Sookmyung Women's University, Seoul 140-742, Republic of Korea.
Hongyu ZhangCancer Epigenetics and Gene Therapy Group, Shanghai Cancer Institute, Shanghai Jiaotong University, Shanghai 200032, China.
Xiaobin LvCenter of Medical Research, Sun Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China.
Kelong MaCancer Epigenetics and Gene Therapy Group, Shanghai Cancer Institute, Shanghai Jiaotong University, Shanghai 200032, China.
Fengxi SuDepartment of Breast Surgery, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China.
Jong Hoon ParkDepartment of Biological Science, Sookmyung Women's University, Seoul 140-742, Republic of Korea. Electronic address: parkjh@sookmyung.ac.kr.
Erwei SongDepartment of Breast Surgery, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China; School of Life Sciences, Sun-Yat-Sen University, Guangzhou 510006, China. Electronic address: songerwei02@yahoo.com.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-initiating cells (T-ICs), a subpopulation of cancer cells with stem cell-like properties, are related to tumor relapse and metastasis. Our previous studies identified a distinct profile of microRNA (miRNA) expression in breast T-ICs (BT-ICs), and the dysregulated miRNAs contribute to the self-renewal and tumorigenesis of these cells. However, the underlying mechanisms for miRNA dysregulation in BT-ICs remain obscure. In the present study, we demonstrated that the expression and function of miR-34c were reduced in the BT-ICs of MCF-7 and SK-3rd cells, a breast cancer cell line enriched for BT-ICs. Ectopic expression of miR-34c reduced the self-renewal of BT-ICs, inhibited epithelial-mesenchymal transition, and suppressed migration of the tumor cells via silencing target gene Notch4. Furthermore, we identified a single hypermethylated CpG site in the promoter region of miR-34c gene that contributed to transcriptional repression of miR-34c in BT-ICs by reducing DNA binding activities of Sp1. Therefore, miR-34c reduction in BT-ICs induced by a single hypermethylated CpG site in the promoter region promotes self-renewal and epithelial-mesenchymal transition of BT-ICs.

Indexed as

Breast NeoplasmsCell DifferentiationCell Line, TumorCell MovementCpG IslandsDNA MethylationDown-RegulationEpithelial-Mesenchymal TransitionHumansMicroRNAsNeoplastic Stem CellsPromoter Regions, GeneticProto-Oncogene ProteinsReceptor, Notch4Receptors, NotchSp1 Transcription FactorMicroRNAsMIRN34 microRNA, humanNOTCH4 protein, humanProto-Oncogene ProteinsReceptor, Notch4Receptors, NotchSp1 Transcription Factor

Identifiers

PMID22074923
PMCPMC3249099

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.