Evidence map›Paper›PMID 25723737›Full record

ReviewInternational journal of molecular sciences2015

Tumor progression locus 2 (Tpl2) kinase as a novel therapeutic target for cancer: double-sided effects of Tpl2 on cancer.

Hye Won Lee, Han Yong Choi, Kyeung Min Joo, Do-Hyun Nam

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 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
1.8field-weighted citation impact, top 17% 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, 38 citations in OpenAlex.

  1. Article
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  6. Tanshinone IIA Inhibits Osteosarcoma Growth through a Src Kinase-Dependent Mechanism.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  7. Review
  8. Review
  9. The combination ofProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Article
  11. Article
  12. Frontiers in chemistry · 2019
    Review
  13. Article
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  15. Article
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  17. Article
  18. miR-589-5p inhibits MAP3K8 and suppresses CD90Journal of experimental & clinical cancer research : CR · 2016
    Article
  19. 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

4 authors at 2 institutions in 1 country.

Hye Won LeeDepartment of Neurosurgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, 135-710 Seoul, Korea. hanyong.choi@samsung.com.
Han Yong ChoiDepartment of Urology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 135-710 Seoul, Korea. hanyong.choi@samsung.com.
Kyeung Min JooDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, 135-710 Seoul, Korea. kmjoo@skku.edu.
Do-Hyun NamDepartment of Neurosurgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, 135-710 Seoul, Korea. nsnam@skku.edu.
Samsung Medical Center · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor progression locus 2 (Tpl2) is a mitogen-activated protein kinase (MAPK) kinase kinase (MAP3K) that conveys various intra- and extra-cellular stimuli to effector proteins of cells provoking adequate adoptive responses. Recent studies have elucidated that Tpl2 is an indispensable signal transducer as an MAP3K family member in diverse signaling pathways that regulate cell proliferation, survival, and death. Since tumorigenesis results from dysregulation of cellular proliferation, differentiation, and apoptosis, Tpl2 participates in many decisive molecular processes of tumor development and progression. Moreover, Tpl2 is closely associated with cytokine release of inflammatory cells, which has crucial effects on not only tumor cells but also tumor microenvironments. These critical roles of Tpl2 in human cancers make it an attractive anti-cancer therapeutic target. However, Tpl2 contradictorily works as a tumor suppressor in some cancers. The double-sided effects of Tpl2 originate from the specific upstream and downstream signaling environment of each tumor, since Tpl2 interacts with various signaling components. This review summarizes recent studies concerning the possible roles of Tpl2 in human cancers and considers its possibility as a therapeutic target, against which novel anti-cancer agents could be developed.

Indexed as

Signal TransductionCytokinesDisease ProgressionHumansImmune SystemInflammation MediatorsMAP Kinase Kinase KinasesModels, BiologicalNeoplasmsProto-Oncogene ProteinsTumor MicroenvironmentCytokinesInflammation MediatorsMAP3K8 protein, humanMAP Kinase Kinase KinasesProto-Oncogene Proteins

Identifiers

PMID25723737
PMCPMC4394431
OpenAlexW2084290127

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.