Evidence map›Paper›PMID 26666820›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

MiRNA-21 induces epithelial to mesenchymal transition and gemcitabine resistance via the PTEN/AKT pathway in breast cancer.

Zhen-Hua Wu, Zhong-Hua Tao, Jian Zhang, Ting Li, Chen Ni, Jie Xie, Jin-Feng Zhang, Xi-Chun Hu

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 98 citations in OpenAlex.

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  13. Human esophageal fibroblast-derived exosomal miR-21 reduced the cisplatin sensitivity to esophageal carcinoma EC9706 cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
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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 2 institutions in 1 country.

Zhen-Hua WuDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China.
Zhong-Hua TaoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China.
Jian ZhangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China.
Ting LiDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China.
Chen NiDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China.
Jie XieDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China.
Jin-Feng ZhangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China.
Xi-Chun HuDepartment of Medical Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, 270 Dong-An Rd, Shanghai, 200032, China. huxichun@aliyun.com.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquisition of gemcitabine resistance in breast cancer has not been fully clarified. Prior studies suggest that miRNAs are important to chemoresistance in solid tumors and we confirmed that miR-21 is involved in the development of gemcitabine resistance. Epithelial-to-mesenchymal transition (EMT) and AKT pathway activation were noted to be important to this resistance as well. PTEN, a direct target gene of miR-21, was significantly downregulated in gemcitabine-resistant breast cancer cells and restoration of PTEN expression blocked miR-21-induced EMT and gemcitabine resistance. Our data offer novel insight into gemcitabine resistance in breast cancer and suggest that miR-21 may be used to predict optimal breast cancer therapy and may be a potential therapeutic target for reversing gemcitabine resistance.

Indexed as

AnimalsAntimetabolites, AntineoplasticBreast NeoplasmsCell Line, TumorCell MovementDeoxycytidineDown-RegulationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGemcitabineGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceMice, Inbred BALB CAKT1 protein, humanAntimetabolites, AntineoplasticDeoxycytidineGemcitabineMicroRNAsMIRN21 microRNA, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRNA, NeoplasmRNA, Small InterferingBreast cancerEpithelial to mesenchymal transition (EMT)Gemcitabine resistancemiR-21

Identifiers

PMID26666820
OpenAlexW2209935799

What OpenQuestion holds

Textmetadata
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.