Evidence map›Paper›PMID 26246283›Full record

ArticleBMB reports2016

Enhancement of paclitaxel-induced breast cancer cell death via the glycogen synthase kinase-3β-mediated B-cell lymphoma 2 regulation.

Kyung Tae Noh, Gil Sun Cha, Tae Heung Kang, Joon Cho, In Duk Jung, Kwang-Youn Kim, Soon-Cheol Ahn, Ji Chang You, Yeong-Min Park

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMB reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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.

Kyung Tae NohDepartment of Infectious Diseases, Armed Forces Medical Research Institute, Daejeon 34059, Korea.
Gil Sun ChaDepartment of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University, Chungju 27478, Korea.
Tae Heung KangDepartment of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University, Chungju 27478, Korea.
Joon ChoDepartment of Neurosurgery, Konkuk University Hospital, Seoul 05030, Korea.
In Duk JungDepartment of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University, Chungju 27478, Korea.
Kwang-Youn KimSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Korea.
Soon-Cheol AhnDepartment of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan 50612, Korea.
Ji Chang YouNational Research Laboratory of Molecular Virology, Department of Pathology, School of Medicine, The Catholic University of Korea, Seoul 03083, Korea.
Yeong-Min ParkDepartment of Immunology, KU Open Innovation Center, College of Medicine, Konkuk University, Chungju 27478, Korea.
Catholic University of Korea · KRPusan National University · KRUlsan National Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine protein kinase that is known to mediate cancer cell death. Here, we show that B-cell lymphoma 2 (Bcl-2), an anti-apoptotic protein, is regulated by GSK-3β and that GSK-3β-mediated regulation of Bcl-2 is crucial for mitochondrial-dependent cell death in paclitaxel-stimulated cells. We demonstrate that MCF7 GSK-3β siRNA cells are more sensitive to cell death than MCF7 GFP control cells and that in the absence of GSK-3β, Bcl-2 levels are reduced, a result enhanced by paclitaxel. Paclitaxel-induced JNK (c-Jun N-terminal kinase) activation is critical for Bcl-2 modulation. In the absence of GSK-3β, Bcl-2 was unstable in an ubiquitination-dependent manner in both basal- and paclitaxeltreated cells. Furthermore, we demonstrate that GSK-3β-mediated regulation of Bcl-2 influences cytochrome C release and mitochondrial membrane potential. Taken together, our data suggest that GSK-3β-dependent regulation of Bcl-2 is crucial for mitochondria-dependent cell death in paclitaxel-mediated breast cancer therapy.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisCytochromes cDNA FragmentationEnzyme ActivationGene Expression Regulation, EnzymologicGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansJNK Mitogen-Activated Protein KinasesMCF-7 CellsMembrane Potential, MitochondrialMitochondriaPaclitaxelProtein StabilityProto-Oncogene Proteins c-bcl-2Antineoplastic Agents, PhytogenicCytochromes cGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanJNK Mitogen-Activated Protein KinasesPaclitaxelProto-Oncogene Proteins c-bcl-2RNA, Small Interfering

Identifiers

PMID26246283
PMCPMC4914213
OpenAlexW1062465693

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.