Evidence map›Paper›PMID 26720004›Full record

ArticlePloS one2015

Bay 61-3606 Sensitizes TRAIL-Induced Apoptosis by Downregulating Mcl-1 in Breast Cancer Cells.

So-Young Kim, Sang Eun Park, Sang-Mi Shim, Sojung Park, Kyung Kon Kim, Seong-Yun Jeong, Eun Kyung Choi, Jung Jin Hwang, Dong-Hoon Jin, Christopher Doosoon Chung and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. Review
  8. Mcl-1 Protein and Viral Infections: A Narrative Review.International journal of molecular sciences · 2024
    Review
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  10. Article
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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

11 authors at 4 institutions in 1 country.

So-Young KimASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Sang Eun ParkASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Sang-Mi ShimDepartment of Biomedical Sciences, Seoul National University, Seoul, Republic of Korea.
Sojung ParkASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Kyung Kon KimASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Seong-Yun JeongASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Eun Kyung ChoiDepartment of Radiation Oncology, ASAN Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Jung Jin HwangASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Dong-Hoon JinDepartment of Convergence Medicine, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Christopher Doosoon ChungASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Inki KimASAN Institute for Life Sciences, ASAN Medical Center, Seoul, Republic of Korea.
Asan Medical Center · KRUlsan College · KRUniversity of Ulsan · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer cells generally develop resistance to TNF-Related Apoptosis-Inducing Ligand (TRAIL) and, therefore, assistance from sensitizers is required. In our study, we have demonstrated that Spleen tyrosine kinase (Syk) inhibitor Bay 61-3606 was identified as a TRAIL sensitizer. Amplification of TRAIL-induced apoptosis by Bay 61-3606 was accompanied by the strong activation of Bak, caspases, and DNA fragmentation. In mechanism of action, Bay 61-3606 sensitized cells to TRAIL via two mechanisms regulating myeloid cell leukemia sequence-1 (Mcl-1). First, Bay 61-3606 triggered ubiquitin-dependent degradation of Mcl-1 by regulating Mcl-1 phosphorylation. Second, Bay 61-3606 downregulates Mcl-1 expression at the transcription level. In this context, Bay 61-3606 acted as an inhibitor of Cyclin-Dependent Kinase (CDK) 9 rather than Syk. In summary, Bay 61-3606 downregulates Mcl-1 expression in breast cancer cells and sensitizes cancer cells to TRAIL-mediated apoptosis.

Indexed as

ApoptosisBreast NeoplasmsCaspasesCell LineCell Line, TumorCyclin-Dependent KinasesDNA FragmentationDown-RegulationFemaleHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsMCF-7 CellsMyeloid Cell Leukemia Sequence 1 ProteinNiacinamideProtein-Tyrosine Kinases2-(7-(3,4-dimethoxyphenyl)imidazo(1,2-c)pyrimidin-5-ylamino)nicotinamideCaspasesCyclin-Dependent KinasesIntracellular Signaling Peptides and ProteinsMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinNiacinamideProtein-Tyrosine KinasesPyrimidinesSyk KinaseSYK protein, humanTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID26720004
PMCPMC4697837
OpenAlexW2203139256

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Registered trials

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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.