Evidence map›Paper›PMID 22387047›Full record

ArticleBiochemical pharmacology2012

Antitumor activity of a novel STAT3 inhibitor and redox modulator in non-small cell lung cancer cells.

Xiaoying Liu, Wei Guo, Shuhong Wu, Li Wang, Ji Wang, Bingbing Dai, Edward S Kim, John V Heymach, Michael Wang, Luc Girard and 4 more

Abstract read
In one paragraph

Article in Biochemical pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 31 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

14 authors at 3 institutions in 1 country.

Xiaoying LiuDepartment of Thoracic and Cardiovascular Surgery, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Wei Guo
Shuhong Wu
Li Wang
Ji Wang
Bingbing Dai
Edward S Kim
John V Heymach
Michael Wang
Luc Girard
John Minna
Jack A Roth
Stephen G Swisher
Bingliang Fang
The University of Texas MD Anderson Cancer Center · USSouthwestern Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HEYMACH, JOHN V., MINNA, JOHN D. · 1996 to 2024
$57.4M
Oncolytic adenovector-mediated TRAIL gene therapy for cancersR01CA092487 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FANG, BINGLIANG · 2002 to 2011
$2.4M
Novel CTD inhibitors with synthetic lethality to oncogenic Ras for cancer therapyR01CA124951 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FANG, BINGLIANG · 2010 to 2013
$1.2M
NCI NIH HHS CA-016672NCI NIH HHS CA070907NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS R01 CA092481NCI NIH HHS R01 CA092487NCI NIH HHS R01 CA124951
6 · The paper itself

Abstract

NSC-743380 is a novel STAT3 inhibitor that suppresses the growth of several NCI-60 cancer cell lines derived from different tissues and induces regression of xenograft tumors in vivo at various doses. To evaluate the antitumor activity of NSC-743380 in lung cancer cells, we analyzed the susceptibility of 50 NSCLC cell lines to this compound using cell viability assay. About 32% (16 of 50) of these cell lines were highly susceptible to this compound, with a 50% inhibitory concentration (IC₅₀) of < 1 μM. In mechanistic studies, the increased numbers of apoptotic cells as well as increased PARP cleavage showed that cytotoxic effects correlate with apoptosis induction. Treatment with NSC-743380 inhibited transcription factor STAT3 activation and induced ROS production in sensitive human lung cancer cell lines but not in resistant cells. Blocking ROS generation with the antioxidant NDGA dramatically abolished NSC-743380-induced growth suppression and apoptosis, but had minimal effect on NSC-743380-induced STAT3 inhibition, suggesting that STAT3 inhibition is not caused by ROS production. Interestingly, knockdown of STAT3 with use of shSTAT3 induced ROS generation and suppressed tumor cell growth. Moreover, scavenging ROS induced by STAT3 inhibition also diminished antitumor activity of STAT3 inhibition. In vivo administration of NSC-743380 suppressed tumor growth and p-STAT3 in lung tumors. Our results indicate that NSC-743380 is a potent anticancer agent for lung cancer and that its apoptotic effects in lung cancer cells are mediated by induction of ROS through STAT3 inhibition.

Indexed as

Carcinoma, Non-Small-Cell LungCell Line, TumorHumansLung NeoplasmsOxidation-ReductionReactive Oxygen SpeciesSTAT3 Transcription FactorReactive Oxygen SpeciesSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID22387047
PMCPMC3391570
OpenAlexW2085806220

What OpenQuestion holds

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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.