Evidence map›Paper›PMID 19737957›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009

Putative tumor-suppressive function of Kruppel-like factor 4 in primary lung carcinoma.

Wenxian Hu, Wayne L Hofstetter, Hong Li, Yanbin Zhou, Yong He, Abujiang Pataer, Li Wang, Keping Xie, Stephen G Swisher, Bingliang Fang

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

74 citing papers in PubMed, 117 citations in OpenAlex.

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  11. Pluripotency Stemness and Cancer: More Questions than Answers.Advances in experimental medicine and biology · 2022
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  13. The Impact of Iron Chelators on the Biology of Cancer Stem Cells.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
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  20. Review

14 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 2 countries.

Wenxian HuSir Run Run Shaw Hospital, Zhejiang University, Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, People's Republic of China.
Wayne L Hofstetter
Hong Li
Yanbin Zhou
Yong He
Abujiang Pataer
Li Wang
Keping Xie
Stephen G Swisher
Bingliang Fang
The University of Texas MD Anderson Cancer Center · USZhejiang University · CNSir Run Run Shaw Hospital · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 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
NCI NIH HHS 3P30CA016672-32S3NCI NIH HHS 5P50CA070907-100007NCI NIH HHS 5R01CA092487-05NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS R01 CA092487
6 · The paper itself

Abstract

purposeKrüppel-like factor 4 (KLF4) is a zinc-finger protein that plays important roles in stem cells and the development of gastric cancers. However, the role of KLF4 in primary lung cancer is unknown. The purpose of this study is to determine possible roles of KLF4 in lung cancer. EXPERIMENTAL

designThe KLF4 expression in primary lung cancer tissues and case-matched normal lung tissues were determined by protein and mRNA analyses. The effects of KLF4 on cell proliferation, clonogenic formation, and cell cycle progression were determined in cultured lung cancer cells or bronchial epithelial cells after enforced KLF4 overexpression or small interfering RNA knockdown. The in vivo antitumor activity of KLF4 was evaluated by using stably transfected lung cancer cells and by adenovector-mediated gene delivery. The effect of KLF4 in regulating p21 and cyclin D1 was also evaluated.

resultsKLF4 protein and mRNA levels were dramatically decreased in most primary lung tumors compared with in case-matched normal lung tissues. Enforced expression of KLF4 resulted in marked inhibition of cell growth and clonogenic formation. The tumor-suppressive effect of KLF4 was associated with its role in up-regulating p21 and down-regulating cyclin D1, leading to cell cycle arrest at the G(1)-S checkpoint. Knockdown of KLF4 promoted cell growth in immortalized human bronchial epithelial cells. The enforced expression of KLF4 gene to lung cancer cells by ex vivo transfection or adenovector-mediated gene transfer suppressed tumor growth in vivo.

conclusionsOur results suggest that KLF4 plays an important role in suppressing the growth of lung carcinoma.

Indexed as

AnimalsCell CycleCell ProliferationCyclin D1Cyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsLung NeoplasmsMiceMice, NudeRNA, MessengerTumor Cells, CulturedCyclin D1Cyclin-Dependent Kinase Inhibitor p21KLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsRNA, Messenger

Identifiers

PMID19737957
PMCPMC2745510
OpenAlexW2163217711

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.