Evidence map›Paper›PMID 22815934›Full record

ArticlePloS one2012

The LKB1 tumor suppressor controls spindle orientation and localization of activated AMPK in mitotic epithelial cells.

Chongjuan Wei, Varun Kumar Bhattaram, John C Igwe, Elizabeth Fleming, Jennifer S Tirnauer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  8. MicroRNA-17 promotes normal ovarian cancer cells to cancer stem cells development via suppression of the LKB1-p53-p21/WAF1 pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  9. Article
  10. Targeting the LKB1 tumor suppressor.Current drug targets · 2014
    Review
  11. Article
  12. Birt-Hogg-Dube syndrome is a novel ciliopathy.Human molecular genetics · 2013
    Article
  13. Review
  14. Article
  15. Review
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 1 country.

Chongjuan WeiDepartment of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Varun Kumar Bhattaram
John C Igwe
Elizabeth Fleming
Jennifer S Tirnauer
UConn Health · USThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Orientation of mitotic spindles plays an integral role in determining the relative positions of daughter cells in a tissue. LKB1 is a tumor suppressor that controls cell polarity, metabolism, and microtubule stability. Here, we show that germline LKB1 mutation in mice impairs spindle orientation in cells of the upper gastrointestinal tract and causes dramatic mislocalization of the LKB1 substrate AMPK in mitotic cells. RNAi of LKB1 causes spindle misorientation in three-dimensional MDCK cell cysts. Maintaining proper spindle orientation, possibly mediated by effects on the downstream kinase AMPK, could be an important tumor suppressor function of LKB1.

Indexed as

MutationAMP-Activated Protein KinasesAnimalsCadherinsCollagenDogsDrug CombinationsEpithelial CellsGenes, Tumor SuppressorLamininMiceMicroscopy, FluorescenceMicrotubulesMitosisProteoglycansRNA InterferenceAMP-Activated Protein KinasesCadherinsCollagenDrug CombinationsLamininmatrigelProteoglycansTjp1 protein, mouseZonula Occludens-1 Protein

Identifiers

PMID22815934
PMCPMC3399794
OpenAlexW2053714758

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.