Evidence map›Paper›PMID 22549160›Full record

ArticleCancer biology & therapy2012

The role of Rac1 in the regulation of NF-κB activity, cell proliferation, and cell migration in non-small cell lung carcinoma.

Adam Gastonguay, Tracy Berg, Andrew D Hauser, Nathan Schuld, Ellen Lorimer, Carol L Williams

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

57 citing papers in PubMed, 96 citations in OpenAlex.

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  14. Rac1 inhibition protects the kidney against kidney ischemia/reperfusion through the inhibition of macrophage migration.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
    Article
  15. Role of ELMO1 in inflammation and cancer-clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2022
    Review
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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.

Adam GastonguayDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA.
Tracy Berg
Andrew D Hauser
Nathan Schuld
Ellen Lorimer
Carol L Williams
Medical College of Wisconsin · US

Funding

Regulation of Ras and Rho Family GTPases in Lung CancerR01CA136799 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI WILLIAMS, CAROL LUCILLE · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA136799
6 · The paper itself

Abstract

The small GTPase Rac1 regulates many cellular processes, including cytoskeletal reorganization, cell migration, proliferation, and survival. Additionally, Rac1 plays a major role in activating NF-κB-mediated transcription. Both Rac1 and NF-κB regulate many properties of the malignant phenotype, including anchorage-independent proliferation and survival, metastasis, and angiogenesis. Despite these findings, the roles of Rac1and NF-κB in non-small cell lung carcinoma, a leading cause of cancer deaths, have not been thoroughly investigated. Here, we compared the effects of Rac1 siRNA to that of the Rac1 inhibitor NSC23766 on multiple features of the NSCLC malignant phenotype, including NF-κB activity. We show that the siRNA-mediated silencing of Rac1 in lung cancer cells results in decreased cell proliferation and migration. The decrease in proliferation was observed in both anchorage-dependent and anchorage-independent assays. Furthermore, cells with decreased Rac1 expression have a slowed progression through the G 1 phase of the cell cycle. These effects induced by Rac1 siRNA correlated with a decrease in NF-κB transcriptional activity. Additionally, inhibition of NF-κB signaling with BAY 11-7082 inhibited proliferation; indicating that the loss of cell proliferation and migration induced by the silencing of Rac1 expression may be attributed in part to loss of NF-κB activity. Interestingly, treatment with the Rac1 inhibitor NSC23766 strongly inhibits cell proliferation, cell cycle progression, and NF-κB activity in lung cancer cells, to an even greater extent than the inhibition induced by Rac1 siRNA. These findings indicate that Rac1 plays an important role in lung cancer cell proliferation and migration, most likely through its ability to promote NF-κB activity, and highlight Rac1 pathways as therapeutic targets for the treatment of lung cancer.

Indexed as

Cell MovementAminoquinolinesCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell ProliferationGene SilencingHumansLung NeoplasmsNF-kappa BNitrilesPyrimidinesrac1 GTP-Binding ProteinSulfonesTranscription, Genetic3-(4-methylphenylsulfonyl)-2-propenenitrileAminoquinolinesNF-kappa BNitrilesNSC 23766Pyrimidinesrac1 GTP-Binding ProteinSulfones

Identifiers

PMID22549160
PMCPMC3408971
OpenAlexW2092585609

What OpenQuestion holds

Textmetadata
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.