Evidence map›Paper›PMID 30844143›Full record

ArticleThe Kaohsiung journal of medical sciences2019

miRNA-192-5p impacts the sensitivity of breast cancer cells to doxorubicin via targeting peptidylprolyl isomerase A.

Yi Zhang, Ying He, Ling-Li Lu, Zheng-Yu Zhou, Neng-Bin Wan, Guo-Peng Li, Xiao He, Hong-Wu Deng

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Yi ZhangThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Ying HeThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Ling-Li LuThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Zheng-Yu ZhouThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Neng-Bin WanThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Guo-Peng LiThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Xiao HeThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Hong-Wu DengThe Second Department of Breast Surgery, Hunan Cancer Hospital, Affiliated Cancer Hospital of Xiangya Medical School, Changsha, China.
Hunan Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The administration of doxorubicin (DOX) is one of the first-line treatments of breast cancer. However, acquisition of resistance remains the major obstacle restricting the clinical application of DOX. MicroRNAs (miRNAs) are small, noncoding RNAs which play crucial role in epigenetic regulation. Recent studies have shown that miRNAs are associated with tumor chemoresistance. Here we aim to explore the role of miRNA-192-5p in resistance to DOX in breast cancer cells. Normal human breast epithelial cell line MCF-10A, breast cancer cell line Michigan Cancer Foundation-7 (MCF-7), and DOX-resistant breast cancer cell line MCF-7/ADR were used here. The expression of miR-192-5p was examined by qPCR, and the expression of peptidylprolyl isomerase A (PPIA) was examined by qPCR and Western blot. The effects of miR-192-5p overexpression on the sensitivity to DOX were confirmed by Methylthiazolyldiphenyl-tetrazolium bromide (MTT) and Annexin-V/PI assay. Downstream molecular mechanisms, including PPIA, BAD, CASP9, Bcl-2, and c-Jun N-terminal kinase (JNK) activation, were detected by Western blot and qPCR. Luciferase reporter assay was used to validate the association between miR-192-5p and PPIA. miR-192-5p was downregulated while PPIA was upregulated in MCF-7/ADR cells. Functionally, miR-192-5p overexpression increased sensitivity to DOX by promoting cell apoptosis. Mechanistically, miR-192-5p overexpression performed its function by activating JNK, augmenting BAD and caspase9 expression, and suppressing Bcl-2 and PPIA expression. Luciferase assay validated that PPIA was a direct target of miR-192-5p. miR-192-5p sensitizes breast cancer cells to DOX by targeting PPIA, suggesting that miR-192-5p might serve as a novel target for reversing DOX resistance and controlling breast tumor growth.

Indexed as

ApoptosisBase SequenceBreast NeoplasmsCell Line, TumorDown-RegulationDoxorubicinFemaleGene Expression Regulation, NeoplasticHumansJNK Mitogen-Activated Protein KinasesMicroRNAsPeptidylprolyl IsomeraseUp-RegulationDoxorubicinJNK Mitogen-Activated Protein KinasesMicroRNAsMIRN192 microRNA, humanPeptidylprolyl Isomerasebreast cancerdoxorubicinmiR-192-5pPPIA

Identifiers

PMID30844143
PMCPMC11900784
OpenAlexW2921455087

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.