Evidence map›Paper›PMID 24312655›Full record

ArticlePloS one2013

Intercellular redistribution of cAMP underlies selective suppression of cancer cell growth by connexin26.

Anjana Chandrasekhar, Edward A Kalmykov, Srikanth R Polusani, Sandra A Mathis, Shoshanna N Zucker, Bruce J Nicholson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Connexins-Therapeutic Targets in Cancers.International journal of molecular sciences · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. The lung communication network.Cellular and molecular life sciences : CMLS · 2015
    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

6 authors at 2 institutions in 1 country.

Anjana ChandrasekharDepartment of Biochemistry, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Edward A Kalmykov
Srikanth R Polusani
Sandra A Mathis
Shoshanna N Zucker
Bruce J Nicholson
The University of Texas Health Science Center at San Antonio · USD'Youville College · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI PETER J HORNSBY · 1995 to 2026
$30.6M
ROLE OF CASPASE-2 IN OSTEOCOLAST APOPTOSIS AGE-EePENDENT OSTEOPOROSISP01AG019316 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HERMAN, BRIAN A. · 2001 to 2011
$11.3M
SELECTIVE PERMEABILITY &PORE STRUCTURE OF GAP JUNCTIONR01GM055437 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI NICHOLSON, BRUCE J · 1997 to 2009
$2.6M
MECHANISMS OF CONTROL OF CELL GROWTH BY GAP JUNCTIONSR01CA048049 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI NICHOLSON, BRUCE J · 1989 to 2003
$1.1M
NCI NIH HHS P30 CA054174NCI NIH HHS P30 CA54174NCI NIH HHS R01 CA048049NIA NIH HHS P01 AG019316NIA NIH HHS P01 AG19316NIA NIH HHS P30 AG013319NIGMS NIH HHS R01 GM055437
6 · The paper itself

Abstract

Connexins (Cx), which constitute gap junction intercellular channels in vertebrates, have been shown to suppress transformed cell growth and tumorigenesis, but the mechanism(s) still remain largely speculative. Here, we define the molecular basis by which Cx26, but less frequently Cx43 or Cx32, selectively confer growth suppression on cancer cells. Functional intercellular coupling is shown to be required, producing partial blocks of the cell cycle due to prolonged activation of several mitogenic kinases. PKA is both necessary and sufficient for the Cx26 induced growth inhibition in low serum and the absence of anchorage. Activation of PKA was not associated with elevated cAMP levels, but appeared to result from a redistribution of cAMP throughout the cell population, eliminating the cell cycle oscillations in cAMP required for efficient cell cycle progression. Cx43 and Cx32 fail to mediate this redistribution as, unlike Cx26, these channels are closed during the G2/M phase of the cell cycle when cAMP levels peak. Comparisons of tumor cell lines indicate that this is a general pattern, with growth suppression by connexins occurring whenever cAMP oscillates with the cell cycle, and the gap junction remain open throughout the cell cycle. Thus, gap junctional coupling, in the absence of any external signals, provides a general means to limit the mitotic rate of cell populations.

Indexed as

Cell CycleCell ProliferationConnexin 26Connexin 43ConnexinsCyclic AMPCyclic AMP-Dependent Protein KinasesGap Junction beta-1 ProteinHeLa CellsHumansConnexin 26Connexin 43ConnexinsCyclic AMPCyclic AMP-Dependent Protein KinasesGap Junction beta-1 ProteinGJB2 protein, human

Identifiers

PMID24312655
PMCPMC3849486
OpenAlexW2094461590

What OpenQuestion holds

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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.