Evidence map›Paper›PMID 29880840›Full record

ArticleCell death & disease2018

RIP1 protects melanoma cells from apoptosis induced by BRAF/MEK inhibitors.

Fu Xi Lei, Lei Jin, Xiao Ying Liu, Fritz Lai, Xu Guang Yan, Margaret Farrelly, Su Tang Guo, Xin Han Zhao, Xu Dong Zhang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% 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, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. SialidaseWorld journal of oncology · 2022
    Article
  6. Review
  7. Advances in RIPK1 kinase inhibitors.Frontiers in pharmacology · 2022
    Review
  8. Article
  9. Two Distinct Faces of Vitamin C: AA vs. DHA.Antioxidants (Basel, Switzerland) · 2021
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Fu Xi LeiDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Lei JinSchool of Medicine and Public Health, The University of Newcastle, Newcastle, NSW, 2308, Australia.
Xiao Ying LiuSchool of Medicine and Public Health, The University of Newcastle, Newcastle, NSW, 2308, Australia.
Fritz LaiSchool of Medicine and Public Health, The University of Newcastle, Newcastle, NSW, 2308, Australia.
Xu Guang YanSchool of Medicine and Public Health, The University of Newcastle, Newcastle, NSW, 2308, Australia.
Margaret FarrellySchool of Medicine and Public Health, The University of Newcastle, Newcastle, NSW, 2308, Australia.
Su Tang GuoSchool of Medicine and Public Health, The University of Newcastle, Newcastle, NSW, 2308, Australia.
Xin Han ZhaoDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China. zhaoxinhan@mail.xjtu.edu.cn.
Xu Dong ZhangSchool of Medicine and Public Health, The University of Newcastle, Newcastle, NSW, 2308, Australia. Xu.Zhang@newcastle.edu.au.ORCID 0000-0001-9457-8003
University of Newcastle Australia · AUFirst Affiliated Hospital of Xi'an Jiaotong University · CNAnhui Medical University · CNShanxi Provincial Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many recent studies have uncovered the necessary role for the receptor-interacting protein kinase 1 (RIP1) in regulating apoptosis and necrosis that cells undergo in response to various cellular stresses. However, the functional significance of RIP1 in promoting cancer cells survival remains poorly understood. Here, we report that RIP1 was upregulated and contributed to both intrinsic and acquired resistance of melanoma cells to BRAF/MEK inhibitors through activation of NF-κB. Strikingly, Snail1-mediated suppression of CYLD played a crucial role in promoting RIP1 expression upon ERK activation, particularly, in melanoma cells with acquired resistance to BRAF inhibitors. In addition, RIP1 kinase activity was not required for melanoma cells to survive BRAF/MEK inhibition as RIP1 mediated NF-κB activation through its intermediate domain. Collectively, our findings reveal that targeting RIP1 in combination with BRAF/MEK inhibitors is a potential approach in the treatment of the disease.

Indexed as

CytoprotectionApoptosisCell Line, TumorDeubiquitinating Enzyme CYLDDrug Resistance, NeoplasmHumansIndolesMelanomaMitogen-Activated Protein Kinase KinasesModels, BiologicalNF-kappa BNuclear Pore Complex ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins B-rafRNA-Binding ProteinsSnail Family Transcription FactorsAGFG1 protein, humanCYLD protein, humanDeubiquitinating Enzyme CYLDIndolesMitogen-Activated Protein Kinase KinasesNF-kappa BNuclear Pore Complex ProteinsPLX 4720Protein Kinase InhibitorsProto-Oncogene Proteins B-rafRNA-Binding ProteinsSnail Family Transcription FactorsSulfonamides

Identifiers

PMID29880840
PMCPMC5992182
OpenAlexW2806377052

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.