Evidence map›Paper›PMID 22410778›Full record

ArticleOncogene2013

Oncogenic K-ras expression is associated with derangement of the cAMP/PKA pathway and forskolin-reversible alterations of mitochondrial dynamics and respiration.

R Palorini, D De Rasmo, M Gaviraghi, L Sala Danna, A Signorile, C Cirulli, F Chiaradonna, L Alberghina, S Papa

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Guideline
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  5. Review
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  7. Article
  8. The bioenergetic landscape of cancer.Molecular metabolism · 2024
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  15. Article
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  17. GPharmacological reviews · 2021
    Review
  18. Review
  19. Article
  20. Mitophagy in Pancreatic Cancer.Frontiers in oncology · 2021
    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

9 authors at 3 institutions in 1 country.

R PaloriniDepartment of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy.
D De Rasmo
M Gaviraghi
L Sala Danna
A Signorile
C Cirulli
F Chiaradonna
L Alberghina
S Papa
University of Milano-Bicocca · ITUniversity of Bari Aldo Moro · ITInstitute of Biomembranes, Bioenergetics and Molecular Biotechnologies · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Warburg effect in cancer cells has been proposed to involve several mechanisms, including adaptation to hypoxia, oncogenes activation or loss of oncosuppressors and impaired mitochondrial function. In previous papers, it has been shown that K-ras transformed mouse cells are much more sensitive as compared with normal cells to glucose withdrawal (undergoing apoptosis) and present a high glycolytic rate and a strong reduction of mitochondrial complex I. Recent observations suggest that transformed cells have a derangement in the cyclic adenosine monophosphate/cAMP-dependent protein kinase (cAMP/PKA) pathway, which is known to regulate several mitochondrial functions. Herein, the derangement of the cAMP/PKA pathway and its impact on transformation-linked changes of mitochondrial functions is investigated. Exogenous stimulation of PKA activity, achieved by forskolin treatment, protected K-ras-transformed cells from apoptosis induced by glucose deprivation, enhanced complex I activity, intracellular adenosine triphosphate (ATP) levels, mitochondrial fusion and decreased intracellular reactive oxygen species (ROS) levels. Several of these effects were almost completely prevented by inhibiting the PKA activity. Short-time treatment with compounds favoring mitochondrial fusion strongly decreased the cellular ROS levels especially in transformed cells. These findings support the notion that glucose shortage-induced apoptosis, specific of K-ras-transformed cells, is associated to a derangement of PKA signaling that leads to mitochondrial complex I decrease, reduction of ATP formation, prevalence of mitochondrial fission over fusion, and thereby opening new approaches for development of anticancer drugs.

Indexed as

Adenosine TriphosphateAnimalsApoptosisCell Line, TumorCell ProliferationCell RespirationCell SurvivalCell Transformation, NeoplasticColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesFibroblastsGene Expression Regulation, NeoplasticGenes, rasGlucoseHumansAdenosine TriphosphateColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesGlucoseReactive Oxygen Species

Identifiers

PMID22410778
OpenAlexW2024612673

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.