Evidence map›Paper›PMID 24792998›Full record

ArticleGynecologic oncology2014

Expression and transcriptional profiling of the LKB1 tumor suppressor in cervical cancer cells.

Xiaoli Zhang, Hanxiang Chen, Xiao Wang, Weiming Zhao, Jason J Chen

Abstract read
In one paragraph

Article in Gynecologic oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Comprehensively Testing the Function of Missense Variation in thebioRxiv : the preprint server for biology · 2025
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  13. Low LKB1 Expression Results in Unfavorable Prognosis in Prostate Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  14. Mir-155 promotes cervical cancer cell proliferation through suppression of its target gene LKB1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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

5 authors at 2 institutions in 2 countries.

Xiaoli ZhangDepartment of Microbiology, Shandong University School of Medicine, Jinan, Shandong, China; Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01532, USA.
Hanxiang ChenDepartment of Microbiology, Shandong University School of Medicine, Jinan, Shandong, China.
Xiao WangDepartment of Pathology, Shandong University School of Medicine, Jinan, Shandong, China.
Weiming ZhaoDepartment of Microbiology, Shandong University School of Medicine, Jinan, Shandong, China. Electronic address: zhaowm@sdu.edu.cn.
Jason J ChenDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA 01532, USA; Cancer Research Center, Shandong University School of Medicine, Jinan, Shandong, China. Electronic address: Jason.chen@umassmed.edu.
Shandong University · CNUniversity of Massachusetts Chan Medical School · US

Funding

Induction of genomic instability by HPV E6 and E7R01CA119134 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CHEN, JASON J · 2008 to 2012
$1.5M
NCI NIH HHS 01CA119134NCI NIH HHS R01 CA119134
6 · The paper itself

Abstract

objectivesTo characterize the biological activities of LKB1, examine LKB1 protein expression and identify LKB1-regulated genes that may serve as therapeutic targets in cervical cancer.

methodsProliferation of cervical cancer HeLa cells expressing LKB1 was examined. LKB1 expression in normal cervical tissues and cervical cancers was assessed by immunohistochemistry. Gene expression profiles of cervical cancer HeLa cells stably expressing LKB1 were analyzed by microarray. Differentially expressed genes were analyzed using Gene Ontology (GO) terms and the Kyoto Encyclopedia of Genes and Genomes (KEGG) PATHWAY database. Quantitative RT-PCR was used to validate the microarray data. The expression of lipid phosphatase inositol polyphosphate 4-phosphatase type II (INPP4B) was confirmed by western blotting.

resultsExpression of LKB1 inhibited HeLa cell proliferation, activated AMPK and was lost in more than 50% of cervical carcinomas. More than 200 genes were differentially expressed between HeLa cells with and without LKB1. Bioinformatics analysis with GO annotation indicated that LKB1 plays a role in receiving diverse stimuli and converting them into molecular signals. KEGG PATHWAY analysis showed that 8 pathways were significantly regulated. These include arginine and proline metabolism and inositol phosphate metabolism. The differential expression of 7 randomly selected genes was confirmed by quantitative RT-PCR. Furthermore, the steady-state level of INPP4B protein was up-regulated in LKB1-overexpressing cells.

conclusionsThis study establishes LKB1 as an important tumor suppressor in cervical cancer and sheds light on a novel signaling pathway regulated by LKB1.

Indexed as

Gene Expression ProfilingAMP-Activated Protein Kinase KinasesFemaleHumansProtein Serine-Threonine KinasesTumor Cells, CulturedUterine Cervical NeoplasmsAMP-Activated Protein Kinase KinasesProtein Serine-Threonine KinasesSTK11 protein, humanCervical carcinomaGene expression profilingINPP4BLKB1Phosphatidyl inositol signaling

Identifiers

PMID24792998
PMCPMC4712024
OpenAlexW2047677537

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.