Evidence map›Paper›PMID 24416428›Full record

ArticlePloS one2014

Induction of chemoresistance by all-trans retinoic acid via a noncanonical signaling in multiple myeloma cells.

Zhiqiang Liu, Tao Li, Kesheng Jiang, Qiaoli Huang, Yicheng Chen, Feng Qian

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

2 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
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

6 authors at 4 institutions in 2 countries.

Zhiqiang LiuDepartment of Lymphoma and Myeloma, Division of Cancer Medicine, Center for Cancer Immunology Research, the University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Tao LiDepartment of Biology, College of Chemistry and Life Sciences, Zhejiang Normal University, Jinhua, Zhejiang, China.
Kesheng JiangDepartment of Biology, College of Chemistry and Life Sciences, Zhejiang Normal University, Jinhua, Zhejiang, China.
Qiaoli HuangDepartment of Biology, College of Chemistry and Life Sciences, Zhejiang Normal University, Jinhua, Zhejiang, China.
Yicheng ChenDepartment of Urology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Feng QianDepartment of Medical Function, Medical School of Yangtze University, Jingzhou, Hubei, China.
Zhejiang Normal University · CNThe University of Texas MD Anderson Cancer Center · USYangtze University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the successful application of all-trans retinoic acid (ATRA) in multiple myeloma treatment, ATRA-induced chemoresistance in the myeloma patients is very common in clinic. In this study, we evaluated the effect of ATRA on the expression of apurinic endonuclease/redox factor-1 (Ape/Ref-1) in the U266 and RPMI-8226 myeloma cells to explore the chemoresistance mechanism involved. ATRA treatment induced upregulation of Ape/Ref-1 via a noncanonical signaling pathway, leading to enhanced pro-survival activity counteracting melphalan (an alkylating agent). ATRA rapidly activated p38-MSK (mitogen- and stress activated protein kinase) cascade to phosphorylate cAMP response element-binding protein (CREB). Phosphorylated CREB was recruited to the Ape/Ref-1 promoter to evoke the gene expression. The stimulation of ATRA on Ape/Ref-1 expression was attenuated by either p38-MSK inhibitors or overexpression of dominant-negative MSK1 mutants. Moreover, ATRA-mediated Ape/Ref-1 upregulation was correlated with histone modification and activation of CBP/p300, an important cofactors for CREB transcriptional activity. C646, a competitive CBP/p300 inhibitor, abolished the upregulation of Ape/Ref-1 induced by ATRA. Intriguingly, CBP rather than p300 played a dominant role in the expression of Ape/Ref-1. Hence, our study suggests the existence of a noncanonical mechanism involving p38-MSK-CREB cascade and CBP induction to mediate ATRA-induced Ape/Ref-1 expression and acquired chemoresistance in myeloma cells.

Indexed as

Drug Resistance, NeoplasmSignal TransductionApoptosisCell DeathCell Line, TumorCell ProliferationCyclic AMP Response Element-Binding ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseGene Expression Regulation, NeoplasticHumansMelphalanMultiple Myelomap300-CBP-Associated Factorp300-CBP Transcription Factorsp38 Mitogen-Activated Protein KinasesPhosphorylationAPEX1 protein, humanCyclic AMP Response Element-Binding ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseMelphalanmitogen and stress-activated protein kinase 1p300-CBP-Associated Factorp300-CBP Transcription Factorsp38 Mitogen-Activated Protein KinasesRibosomal Protein S6 Kinases, 90-kDaTretinoin

Identifiers

PMID24416428
PMCPMC3887062
OpenAlexW2107311514

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.