Evidence map›Paper›PMID 20182446›Full record

ArticleThe Journal of investigative dermatology2010

Induction of autophagy and inhibition of melanoma growth in vitro and in vivo by hyperactivation of oncogenic BRAF.

Nityanand Maddodi, Wei Huang, Thomas Havighurst, KyungMann Kim, B Jack Longley, Vijayasaradhi Setaluri

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. International journal of molecular sciences · 2021
    Article
  6. Review
  7. Growth Inhibitory Signaling of the Raf/MEK/ERK Pathway.International journal of molecular sciences · 2020
    Review
  8. Non-Apoptotic Cell Death Signaling Pathways in Melanoma.International journal of molecular sciences · 2020
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Acetylsalicylic Acid Governs the Effect of Sorafenib inClinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  14. Mechanisms and prevention of UV-induced melanoma.Photodermatology, photoimmunology & photomedicine · 2018
    Review
  15. Review
  16. Treatment with diphenyl-pyrazole compound anle138b/c reveals that α-synuclein protects melanoma cells from autophagic cell death.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. Review
  19. Article
  20. 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 1 institution in 1 country.

Nityanand MaddodiDepartment of Dermatology, UW School of Medicine and Public Health, University of Wisconsin, 1300 University Avenue, Madison, WI 53706, USA.
Wei Huang
Thomas Havighurst
KyungMann Kim
B Jack Longley
Vijayasaradhi Setaluri
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Prognostic Significance of Neuronal Differentiation of Cutaneous MelanomaR21CA125091 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SETALURI, VIJAYASARADHI · 2008 to 2009
$364k
NCI NIH HHS P30 CA014520NCI NIH HHS R21 CA125091
6 · The paper itself

Abstract

Activating mutations in NRAS and BRAF are found frequently in cutaneous melanomas. Because concurrent mutations of both BRAF and RAS are extremely rare, it is thought that transformation by RAS and BRAF occurs through a common mechanism. Also, there is evidence for a relationship of synthetic lethality between NRAS and BRAF oncogenes that leads to selection against cells with a hyperactive mitogen-activated protein kinase (MAPK) pathway. However, it is not known whether the hyperactivation of the MAPK pathway by overexpression of either oncogene alone could also inhibit melanoma tumorigenesis. Here, we show that in melanoma cells with oncogenic BRAF (mBRAF), high levels of mBRAF induce hyperactivation of ERK and senescence-like phenotype and trigger autophagy by inhibiting the mammalian target of rapamycin complex signaling. Growth inhibition and cell death caused by high mBRAF levels are partially rescued by downregulation of BRAF protein or inhibition of autophagy, but not by inhibition of the MAPK or apoptotic pathways. In nude mice, growth of mBRAF-overexpressing tumors is inhibited. Quantitative immunohistochemical analysis of human melanomas and cell lines showed a significant positive correlation between the levels of BRAF protein and autophagy marker light chain 3. Our data suggest that high oncogenic BRAF levels trigger autophagy, which may have a role in melanoma tumor progression.

Indexed as

Cell ProliferationAnimalsApoptosisAutophagyCell CycleCell LineCell Line, TumorCells, CulturedFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMelanomaMicePlasmidsProtein Serine-Threonine KinasesBRAF protein, humanIntracellular Signaling Peptides and ProteinsMTOR protein, humanmTOR protein, mouseProtein Serine-Threonine KinasesProto-Oncogene Proteins B-rafTOR Serine-Threonine Kinases

Identifiers

PMID20182446
PMCPMC2869390
OpenAlexW2087298951

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.