Evidence map›Paper›PMID 28232202›Full record

ArticleFree radical biology & medicine2017

Regulation of STAT3 and NF-κB activations by S-nitrosylation in multiple myeloma.

Jinsu Kim, Seungho Choi, Nishant Saxena, Avtar K Singh, Inderjit Singh, Je-Seong Won

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 24 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

6 authors at 1 institution in 1 country.

Jinsu KimDepartment of Pediatrics, Medical University of South Carolina, Charleston, SC 29425, United States.
Seungho ChoiDepartment of Pediatrics, Medical University of South Carolina, Charleston, SC 29425, United States.
Nishant SaxenaDepartment of Pediatrics, Medical University of South Carolina, Charleston, SC 29425, United States.
Avtar K SinghDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC 29425, United States; Pathology and Laboratory Medicine Service, Ralph H. Johnson Veterans Administration Medical Center, Charleston, SC 29401, United States.
Inderjit SinghDepartment of Pediatrics, Medical University of South Carolina, Charleston, SC 29425, United States. Electronic address: singhi@musc.edu.
Je-Seong WonDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC 29425, United States. Electronic address: wonj@musc.edu.
Medical University of South Carolina · US

Funding

CYTOKINES IN GLIAL CELLS AND EAE BRAINR01NS037766 · NINDS · UNIVERSITY OF NEVADA RENO · PI SINGH, INDERJIT · 1998 to 2019
$5.9M
Nitrosylation Mechanisms for Protection Against Neurovascular Inflammatory InjuryR01NS072511 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SINGH, AVTAR K · 2011 to 2015
$1.6M
Development of S-Nitrosothiol-based Therapy for Alzheimer's DiseaseI01BX001062 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI SINGH, AVTAR K · 2011 to 2014
–
Immunomodulation and Neuroprotection in Multiple SclerosisI01BX002829 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI SINGH, INDERJIT · 2015 to 2025
–
BLRD VA I01 BX001062BLRD VA I01 BX002829NINDS NIH HHS R01 NS037766NINDS NIH HHS R01 NS072511
6 · The paper itself

Abstract

Numerous reports suggest that aberrant activations of STAT3 and NF-κB promote survival and proliferation of multiple myeloma (MM) cells. In the present report, we demonstrate that a synthetic S-nitrosothiol compound, S-nitroso-N-acetylcysteine (SNAC), inhibits proliferation and survival of multiple MM cells via S-nitrosylation-dependent inhibition of STAT3 and NF-κB. In human MM cells (e.g. U266, H929, and IM-9 cells), SNAC treatment increased S-nitrosylation of STAT3 and NF-κB and inhibited their activities. Consequently, SNAC treatment resulted in MM cell cycle arrest at G1/S check point and inhibited their proliferation. SNAC also decreased the expression of cell survival factors and increased the activities of caspases, thus increased sensitivity of MM cells to melphalan, a chemotherapeutic agent for MM. In U266 xenografted mice, SNAC treatment decreased the activity of STAT3 and reduced the growth of human CD138 positive cells (U266 cells) in the bone marrow and also reduced their production of human IgE into the serum. Taken together, these data document the S-nitrosylation mediated inhibition of MM cell proliferation and cell survival via inhibition of STAT3 and NF-κB pathways and its efficacy in animal model of MM.

Indexed as

AcetylcysteineAnimalsApoptosisCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMiceMultiple MyelomaNF-kappa BSignal TransductionSTAT3 Transcription FactorXenograft Model Antitumor AssaysAcetylcysteineNF-kappa BS-nitroso-N-acetylcysteineSTAT3 protein, humanSTAT3 Transcription FactorApoptosisBcl-2CdkCyclinMultiple myelomaNF-κBProliferationS-nitroso-N-acetylcysteine (SNAC)S-nitrosylationSTAT3U266Xenograft

Identifiers

PMID28232202
PMCPMC5826580
OpenAlexW2590547211

What OpenQuestion holds

Textmetadata
LicenceTDM
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.