Evidence map›Paper›PMID 29724992›Full record

ArticleCell death & disease2018

Dicer1 downregulation by multiple myeloma cells promotes the senescence and tumor-supporting capacity and decreases the differentiation potential of mesenchymal stem cells.

Juan Guo, Youshan Zhao, Chengming Fei, Sida Zhao, Qingqing Zheng, Jiying Su, Dong Wu, Xiao Li, Chunkang Chang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

28 citing papers in PubMed, 42 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

9 authors at 2 institutions in 1 country.

Juan GuoDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Youshan ZhaoDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Chengming FeiDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Sida ZhaoDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Qingqing ZhengDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Jiying SuDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Dong WuDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Xiao LiDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Chunkang ChangDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, Shanghai, China. changchunkang@sjtu.edu.cn.
Shanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow mesenchymal stem cells (BMMSCs) facilitate the growth of multiple myeloma (MM) cells, but the underlying mechanisms remain unclear. This study demonstrates that the senescence of MM-MSCs significantly increased, as evidenced by a decrease in proliferation and increase in the number of cells positive for senescence-associated β-galactosidase activity. Senescent MM-MSCs displayed decreased differentiation potential and increased tumor-supporting capacity. Dicer1 knockdown in the MSCs of healthy controls promoted cellular senescence and tumor-supporting capacity, while decreasing the differentiation capacity. Dicer1 overexpression in MM-MSCs reversed the effects on differentiation and reduced cellular senescence. In addition, decreased expression of the microRNA-17 family was identified as a favorable element responsible for increasing senescence, with the expression of p21 increased in Dicer1 knockdown cells. Furthermore, we observed decreased expression of miR-93 and miR-20a in MM-MSCs, while upregulation of miR-93/miR-20a decreased cellular senescence, as evidenced by the increased p21 expression. Importantly, we found that myeloma cells could induce the senescence of MSCs from healthy controls, as observed from the decreased expression of Dicer1 and miR-93/miR-20a and increased expression of p21. Overall, MM cells downregulate Dicer1 in MSCs, which leads to senescence; in turn, senescent MSCs promote MM cell growth, which most likely contributes to disease progression.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAged, 80 and overApoptosisbeta-GalactosidaseCase-Control StudiesCell CycleCell DifferentiationCell ProliferationCellular SenescenceCoculture TechniquesCyclin-Dependent Kinase Inhibitor p21DEAD-box RNA HelicasesFemaleHumansbeta-GalactosidaseCyclin-Dependent Kinase Inhibitor p21DEAD-box RNA HelicasesDICER1 protein, humanMicroRNAsMIRN17 microRNA, humanMIRN20a microRNA, humanMIRN93 microRNA, humanRibonuclease IIIRNA, Small Interfering

Identifiers

PMID29724992
PMCPMC5938708
OpenAlexW2802640733

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.