Evidence map›Paper›PMID 21911617›Full record

ArticleThe Journal of physiology2011

The potassium-chloride cotransporter 2 promotes cervical cancer cell migration and invasion by an ion transport-independent mechanism.

Wei-Chun Wei, Colin J Akerman, Sarah E Newey, Jiliu Pan, Nicholas W V Clinch, Yves Jacob, Meng-Ru Shen, Robert J Wilkins, J Clive Ellory

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. A novel pathogenicFrontiers in molecular neuroscience · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. The Important Role of Ion Transport System in Cervical Cancer.International journal of molecular sciences · 2021
    Review
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  11. Article
  12. Review
  13. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Wei-Chun WeiDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Colin J Akerman
Sarah E Newey
Jiliu Pan
Nicholas W V Clinch
Yves Jacob
Meng-Ru Shen
Robert J Wilkins
J Clive Ellory
University of Oxford · GBInstitut Pasteur · FRNational Cheng Kung University · TW

Funding

Medical Research Council G0601503Medical Research Council G0700759
6 · The paper itself

Abstract

K(+)-Cl(-) cotransporters (KCCs) play a fundamental role in epithelial cell function, both in the context of ionic homeostasis and also in cell morphology, cell division and locomotion. Unlike other ubiquitously expressed KCC isoforms, expression of KCC2 is widely considered to be restricted to neurons, where it is responsible for maintaining a low intracellular chloride concentration to drive hyperpolarising postsynaptic responses to the inhibitory neurotransmitters GABA and glycine. Here we report a novel finding that KCC2 is widely expressed in several human cancer cell lines including the cervical cancer cell line (SiHa). Membrane biotinylation assays and immunostaining showed that endogenous KCC2 is located on the cell membrane of SiHa cells. To elucidate the role of KCC2 in cervical tumuorigenesis, SiHa cells with stable overexpression or knockdown of KCC2 were employed. Overexpression of KCC2 had no significant effect on cell proliferation but dramatically suppressed cell spreading and stress fibre organization, while knockdown of KCC2 showed opposite effects. In addition, insulin-like growth factor 1 (IGF-1)-induced cell migration and invasiveness were significantly increased by overexpression of KCC2. KCC2-induced cell migration and invasion were not dependent on KCC2 transport function since overexpression of an activity-deficient mutant KCC2 still increased IGF-1-induced cell migration and invasion. Moreover, overexpression of KCC2 significantly diminished the number of focal adhesions, while knockdown of KCC2 increased their number. Taken together, our data establish that KCC2 expression and function are not restricted to neurons and that KCC2 serves to increase cervical tumourigenesis via an ion transport-independent mechanism.

Indexed as

Cell MovementCell Line, TumorCell ProliferationFemaleHeLa CellsHumansInsulin-Like Growth Factor IIon TransportK Cl- CotransportersNeoplasm InvasivenessSymportersTransfectionUterine Cervical NeoplasmsInsulin-Like Growth Factor IK Cl- CotransportersSymporters

Identifiers

PMID21911617
PMCPMC3240877
OpenAlexW1636188611

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.