Evidence map›Paper›PMID 24286313›Full record

ArticleBMB reports2014

Establishment and characterization of bortezomib-resistant U266 cell line: constitutive activation of NF-κB-mediated cell signals and/or alterations of ubiquitylation-related genes reduce bortezomib-induced apoptosis.

Juwon Park, Eun-Kyung Bae, Chansu Lee, Jee-Hye Choi, Woo June Jung, Kwang-Sung Ahn, Sung-Soo Yoon

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

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  7. Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018
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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

7 authors at 2 institutions in 1 country.

Juwon ParkCancer Research Institute, Seoul National University College of Medicine, Seoul 110-799, Korea.
Eun-Kyung BaeBiomedical Research Institute, Seoul National University Hospital, Seoul 110-799, Korea.
Chansu LeeCancer Research Institute, Seoul National University College of Medicine, Seoul 110-799, Korea.
Jee-Hye ChoiCancer Research Institute, Seoul National University College of Medicine, Seoul 110-799, Korea.
Woo June JungCancer Research Institute, Seoul National University College of Medicine, Seoul 110-799, Korea.
Kwang-Sung AhnBiomedical Research Institute, Seoul National University Hospital, Seoul 110-799, Korea.
Sung-Soo YoonCancer Research Institute, Seoul National University College of Medicine; Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-799, Korea.
Seoul National University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bortezomib has been known as the most promising anti-cancer drug for multiple myeloma (MM). However, recent studies reported that not all MM patients respond to bortezomib. To overcome such a stumbling-block, studies are needed to clarify the mechanisms of bortezomib resistance. In this study, we established a bortezomib-resistant cell line (U266/velR), and explored its biological characteristics. The U266/velR showed reduced sensitivity to bortezomib, and also showed crossresistance to the chemically unrelated drug thalidomide. U266/velR cells had a higher proportion of CD138 negative subpopulation, known as stem-like feature, compared to parental U266 cells. U266/velR showed relatively less inhibitory effect of prosurvival NF-κB signaling by bortezomib. Further analysis of RNA microarray identified genes related to ubiquitination that were differentially regulated in U266/velR. Moreover, the expression level of CD52 in U266 cells was associated with bortezomib response. Our findings provide the basis for developing therapeutic strategies in bortezomib-resistant relapsed and refractory MM patients.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsApoptosisBoronic AcidsBortezomibCell Line, TumorGene Expression Regulation, NeoplasticHumansMultiple MyelomaNF-kappa BPyrazinesSignal TransductionSyndecan-1ThalidomideUbiquitinationAntineoplastic AgentsBoronic AcidsBortezomibNF-kappa BPyrazinesSDC1 protein, humanSyndecan-1Thalidomide

Identifiers

PMID24286313
PMCPMC4163865
OpenAlexW2090675458

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.