Evidence map›Paper›PMID 29329575›Full record

ArticleBMC cancer2018

MicroRNA-200a confers chemoresistance by antagonizing TP53INP1 and YAP1 in human breast cancer.

San-Jian Yu, Liu Yang, Qi Hong, Xia-Ying Kuang, Gen-Hong Di, Zhi-Ming Shao

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 8% of its field
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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

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  7. The potential role of miR-155 in the tumorigenesis of cervical cancer.Frontiers in cell and developmental biology · 2025
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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

6 authors at 1 institution in 1 country.

San-Jian YuBreast Cancer Institute, Department of Breast Surgery, Cancer Hospital/Cancer Institute, Shanghai Medical College, Institutes of Biomedical Sciences, Fudan University, #270 Dong An Road, Shanghai, 200032, People's Republic of China.
Liu YangBreast Cancer Institute, Department of Breast Surgery, Cancer Hospital/Cancer Institute, Shanghai Medical College, Institutes of Biomedical Sciences, Fudan University, #270 Dong An Road, Shanghai, 200032, People's Republic of China.
Qi HongBreast Cancer Institute, Department of Breast Surgery, Cancer Hospital/Cancer Institute, Shanghai Medical College, Institutes of Biomedical Sciences, Fudan University, #270 Dong An Road, Shanghai, 200032, People's Republic of China.
Xia-Ying KuangBreast Cancer Institute, Department of Breast Surgery, Cancer Hospital/Cancer Institute, Shanghai Medical College, Institutes of Biomedical Sciences, Fudan University, #270 Dong An Road, Shanghai, 200032, People's Republic of China.
Gen-Hong DiBreast Cancer Institute, Department of Breast Surgery, Cancer Hospital/Cancer Institute, Shanghai Medical College, Institutes of Biomedical Sciences, Fudan University, #270 Dong An Road, Shanghai, 200032, People's Republic of China.
Zhi-Ming ShaoBreast Cancer Institute, Department of Breast Surgery, Cancer Hospital/Cancer Institute, Shanghai Medical College, Institutes of Biomedical Sciences, Fudan University, #270 Dong An Road, Shanghai, 200032, People's Republic of China. zhimingshao@yahoo.com.
Fudan University Shanghai Cancer Center · CN

Funding

National Natural Science Foundation of China 81302303
6 · The paper itself

Abstract

backgroundEmerging evidence suggests molecular and phenotypic association between treatment resistance and epithelial-mesenchymal transition (EMT) in cancer. Compared with the well-defined molecular events of miR-200a in EMT, the role of miR-200a in therapy resistance remains to be elucidated.

methodsBreast cancer cells transfected with mimic or inhibitor for miR-200a was assayed for chemoresistance in vitro. miR-200a expression was assessed by quantitative real-time PCR (qRT-PCR) in breast cancer patients treated with preoperative chemotherapy. Luciferase assays, cell proliferation assay were performed to identify the targets of miR-200a and the mechanism by which it promotes treatment resistance. Survival analysis was used to evaluate the prognosis value of miR-200a.

resultsIn this study, our results showed ectopic expression of miR-200a promotes chemoresistance in breast cancer cell lines to several chemotherapeutic agents, whereas inhibition of miR-200a enhances gemcitabine chemosensitivity in resistance cancer cells. We found overexpression of miR-200a was closely associated with poor response to preoperative chemotherapy and poor prognosis in breast cancer patients. Furthermore, knockdown of YAP1 and TP53INP1 phenocopied the effects of miR-200a overexpression, and confirmed that TP53INP1 is a novel target of miR-200a. Remarkably, TP53INP1 expression is inversely correlated with miR-200a expression in Breast cancer cell lines. Taken together, these clinical and experimental results demonstrate that miR-200a is a determinant of chemoresistance of breast cancer.

conclusionsUpregulated miR-200a enhances treatment resistance via antagonizing TP53INP1 and YAP1 in breast cancer.

Indexed as

Breast NeoplasmsCarrier ProteinsCell Cycle ProteinsCell ProliferationDeoxycytidineDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGemcitabineGene Expression Regulation, NeoplasticHeat-Shock ProteinsHumansMCF-7 CellsMicroRNAsNuclear ProteinsPrognosisCarrier ProteinsCell Cycle ProteinsDeoxycytidineGemcitabineHeat-Shock ProteinsMicroRNAsMIRN200 microRNA, humanNuclear ProteinsTP53INP1 protein, humanTranscription FactorsYY1AP1 protein, humanBreast cancerChemoresistancemicroRNAPreoperative chemotherapy

Identifiers

PMID29329575
PMCPMC5766993
OpenAlexW2783460982

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.