Evidence map›Paper›PMID 24520316›Full record

ArticlePloS one2014

CRIF1 interacting with CDK2 regulates bone marrow microenvironment-induced G0/G1 arrest of leukemia cells.

Qian Ran, Ping Hao, Yanni Xiao, Lixing Xiang, Xingde Ye, Xiaojun Deng, Jiang Zhao, Zhongjun Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  11. CRIF1 as a potential target to improve the radiosensitivity of osteosarcoma.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Mitochondrial ribosomes in cancer.Seminars in cancer biology · 2017
    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

8 authors at 2 institutions in 1 country.

Qian RanDepartment of Blood Transfusion, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Ping HaoOncologic Center, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Yanni XiaoDepartment of Blood Transfusion, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Lixing XiangDepartment of Blood Transfusion, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Xingde YeDepartment of Blood Transfusion, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Xiaojun DengDepartment of Blood Transfusion, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Jiang ZhaoDepartment of Blood Transfusion, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Zhongjun LiDepartment of Blood Transfusion, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Xinqiao Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo assess the level of CR6-interacting factor 1 (CRIF1), a cell cycle negative regulator, in patients with leukemia and investigate the role of CRIF1 in regulating leukemia cell cycle.

methodsWe compared the CRIF1 level in bone marrow (BM) samples from healthy and acute myeloid leukemia (AML), iron deficiency anemia (IDA) and AML-complete remission (AML-CR) subjects. We also manipulated CRIF1 level in the Jurkat cells using lentivirus-mediated overexpression or siRNA-mediated depletion. Co-culture with the BM stromal cells (BMSCs) was used to induce leukemia cell cycle arrest and mimic the BM microenvironment.

resultsWe found significant decreases of CRIF1 mRNA and protein in the AML group. CRIF1 overexpression increased the proportion of Jurkat cells arrested in G0/G1, while depletion of endogenous CRIF1 decreased cell cycle arrest. Depletion of CRIF1 reversed BMSCs induced cell cycle arrest in leukemia cells. Co-immunoprecipitation showed a specific binding of CDK2 to CRIF1 in Jurkat cells during cell cycle arrest. Co-localization of two proteins in both nucleus and cytoplasm was also observed with immunofluorescent staining.

conclusionCRIF1 may play a regulatory role in the BM microenvironment-induced leukemia cell cycle arrest possibly through interacting with CDK2 and acting as a cyclin-dependent kinase inhibitor.

Indexed as

Cellular MicroenvironmentG1 Phase Cell Cycle CheckpointsAdolescentAdultAgedAged, 80 and overBone MarrowCase-Control StudiesCell Cycle ProteinsChildCyclin-Dependent Kinase 2FemaleGene Expression Regulation, LeukemicHumansIntracellular SpaceJurkat CellsCDK2 protein, humanCell Cycle ProteinsCyclin-Dependent Kinase 2GADD45GIP1 protein, humanNuclear ProteinsRNA, Messenger

Identifiers

PMID24520316
PMCPMC3919709
OpenAlexW2003594175

What OpenQuestion holds

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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.