Evidence map›Paper›PMID 27857131›Full record

ArticleLeukemia2017

Epigenetic silencing of miR-137 induces drug resistance and chromosomal instability by targeting AURKA in multiple myeloma.

Y Qin, S Zhang, S Deng, G An, X Qin, F Li, Y Xu, M Hao, Y Yang, W Zhou and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2017. 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
6.1field-weighted citation impact, top 3% 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, 114 citations in OpenAlex.

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  8. miR-137: a potential therapeutic target for lung cancer.Frontiers in cell and developmental biology · 2024
    Review
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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

12 authors at 3 institutions in 2 countries.

Y QinDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
S ZhangDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
S DengDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
G AnDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
X QinDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
F LiDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
Y XuDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
M HaoDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
Y YangDivision of Molecular and Cellular Biology, Department of Laboratory Hematology, Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada.
W ZhouDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
H ChangDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
L QiuDepartment of Lymphoma and Myeloma, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, China.
Institute of Hematology & Blood Diseases Hospital · CNUniversity Health Network · CATianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is the second most prevalent hematologic malignancy. Aberrant microRNAs (miRNAs) expression has been shown to be involved in the pathogenesis of MM. In this study, we further demonstrated that miR-137 was significantly downregulated in MM and negatively correlated with clinical prognosis. Moreover, we described the epigenetic regulation of miR-137 and its association with progression-free survival in MM patients. Furthermore, overexpression of miR-137 in MM cell line (miR-137 OE) increased its sensitivity to bortezomib and eprirubicin in vitro. Also, some high-risk genetic abnormalities in MM, including deletion of chromosome 1p22.2, 14q or 17p13, and gain of chromosome 1p22.2 were detected in NCI-H929 empty vector (NCI-H929 EV) treated cells but not in the NCI-H929 miR-137 overexpression (NCI-H929 miR-137 OE) cells. Luciferase reporter assays demonstrated that miR-137 targeted AURKA. Ectopic expression of miR-137 strongly reduced the expression of AURKA and p-ATM/Chk2 in MM cells, and increased the expression of p53, and p21. Importantly, miR-137 overexpression together with bortezomib treatment significantly inhibited tumor growth in MM xenograft model. Taken together, this study demonstrates that miR-137 is epigenetically silenced in MM, and overexpression of miR-137 could reduce drug resistance and overcome chromosomal instability of the MM cells via affecting the apoptosis and DNA damage pathways.

Indexed as

Epigenesis, GeneticGene SilencingAnimalsAurora Kinase ABone MarrowCase-Control StudiesCell Line, TumorChromosomal InstabilityDrug Resistance, NeoplasmFemaleHeterograftsHumansMaleMiceMicroRNAsMiddle AgedAurora Kinase AMicroRNAsMIRN137 microRNA, human

Identifiers

PMID27857131
OpenAlexW2554059528

What OpenQuestion holds

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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.