Evidence map›Paper›PMID 27527856›Full record

ArticleOncotarget2016

Upregulation of miR-181c inhibits chemoresistance by targeting ST8SIA4 in chronic myelocytic leukemia.

Lifen Zhao, Yan Li, Xiaobo Song, Huimin Zhou, Nana Li, Yuan Miao, Li Jia

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

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  12. MicroRNA-181c-5p modulates phagocytosis efficiency in bone marrow-derived macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
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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

7 authors at 2 institutions in 2 countries.

Lifen ZhaoCollege of Laboratory Medicine, Dalian Medical University, Dalian, Liaoning Province, China.
Yan LiDepartment of Clinical Laboratory, the First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China.
Xiaobo SongDepartment of Medical Biology, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway.
Huimin ZhouDepartment of Microbiology, Dalian Medical University, Dalian, Liaoning Province, China.
Nana LiCollege of Laboratory Medicine, Dalian Medical University, Dalian, Liaoning Province, China.
Yuan MiaoCollege of Laboratory Medicine, Dalian Medical University, Dalian, Liaoning Province, China.
Li JiaCollege of Laboratory Medicine, Dalian Medical University, Dalian, Liaoning Province, China.
Dalian Medical University · CNUiT The Arctic University of Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy resistance frequently drives tumor progression. Increased expression of ST8SIA4 has been reported in diverse carcinomas and highly correlates with leukemia multidrug resistance (MDR). MicroRNAs (miRNA) are widely recognized as key players in cancer progression and drug resistance. Here, to explore whether miRNA modulates the sensitivity of chronic myelocytic leukemia (CML) to chemotherapeutic agents and regulates ST8SIA4 expression, we analyzed the complete miRNA expression profile and found a subset of miRNAs specifically dysregulated in adriamycin-resistant CML cell line K562/ADR and its parent cell line K562. Compared with three pairs of CML cell lines and 38 clinical samples of peripheral blood mononuclear cells (PBMC) of CML patients, miR-181c expression was down-regulated in drug-resistant cell lines and CML/MDR samples. Altered expression levels of miR-181c influenced the MDR phenotypes of K562 and K562/ADR. Reporter-gene assay showed that miR-181c directly targeted and inhibited the ST8SIA4 expression, as well as miR-181c was inversely correlated with the levels of ST8SIA4 expression in CML cell lines and samples. Moreover, ST8SIA4 could reverse the effect of miR-181c on drug resistance in K562 and K562/ADR cells in vitro. Upregulation of miR-181c sensitized K562/ADR cells to adriamycin in vivo through directly suppressing ST8SIA4 expression. Further investigation showed that miR-181c mediated the activity of phosphoinositide-3 kinase (PI3K)/AKT signal pathway, and inhibition of PI3K/Akt in K562 cells counteracted miR-181c-mediated MDR phenotype. These data revealed an important role for miR-181c in the regulation of chemoresistance in CML, and suggested the potential application of miR-181c in drug resistance treatment.

Indexed as

Up-RegulationAnimalsAntibiotics, AntineoplasticCell Line, TumorCells, CulturedDoxorubicinDrug Resistance, NeoplasmGene Expression ProfilingGene Expression Regulation, LeukemicHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMice, NudeMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAntibiotics, AntineoplasticDoxorubicinMicroRNAsMIrn181 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSialyltransferasesST8SIA4 protein, humanchemoresistancechronic myelocytic leukemiamiR-181cPI3K/AKTST8SIA4

Identifiers

PMID27527856
PMCPMC5312369
OpenAlexW2497832431

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.