Evidence map›Paper›PMID 24170542›Full record

ArticleMolecular and cellular biochemistry2014

Adhesion to fibronectin induces p27(Kip1) nuclear accumulation through down-regulation of Jab1 and contributes to cell adhesion-mediated drug resistance (CAM-DR) in RPMI 8,226 cells.

Min Fei, Qinglei Hang, Sicong Hou, Songbin He, Changgeng Ruan

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Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

9 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Min FeiJiangsu Institute of Hematology, The First Affiliated Hospital, Soochow University, Suzhou, Jiangsu, China.
Qinglei Hang
Sicong Hou
Songbin He
Changgeng Ruan

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence has been shown that integrin-mediated cellular adhesion confers resistance to chemotherapy of multiple myeloma. The molecular mechanism underlying cell adhesion-mediated drug resistance (CAM-DR) is, however, poorly understood. In this report, we demonstrated that RPMI 8,226 cells accumulated p27(Kip1) in the nucleus when they were adhered to fibronectin (FN). The adhesion-mediated p27(Kip1) nuclear recruitment was regulated via the down-regulation of Jab1, a negative regulator of cell cycle. Overexpression of Jab1 reversed the elevated p27(Kip1) in the nucleus, which needed phosphorylation of p27(Kip1) on Serine 10, whereas inhibition of Jab1 by siRNA further increased the elevated p27(Kip1). Furthermore, we found overexpression of Jab1 did not affect 8,226 cells adhesion to FN, but reversed doxorubicin or mitoxantrone-induced CAM-DR phenotype. In conclusion, our data suggest that Jab1 plays an important role in CAM-DR, which depends on pSer10-p27(Kip1)-mediated subcellular localization of p27(Kip1). The understanding of this novel molecular mechanism may prove valuable in designing new therapeutic approaches for CAM-DR in Multiple myeloma.

Indexed as

Cell AdhesionDown-RegulationCell Line, TumorCell NucleusCOP9 Signalosome ComplexCyclin-Dependent Kinase Inhibitor p27Drug Resistance, NeoplasmFibronectinsHumansIntracellular Signaling Peptides and ProteinsMicroscopy, FluorescenceMultiple MyelomaPeptide HydrolasesPhosphorylationCDKN1B protein, humanCOP9 Signalosome ComplexCOPS5 protein, humanCyclin-Dependent Kinase Inhibitor p27FibronectinsIntracellular Signaling Peptides and ProteinsPeptide Hydrolases

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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.