Evidence map›Paper›PMID 26083935›Full record

ReviewCancers2015

Involvement of 14-3-3 Proteins in Regulating Tumor Progression of Hepatocellular Carcinoma.

Yi-Ju Wu, Yee-Jee Jan, Bor-Sheng Ko, Shu-Man Liang, Jun-Yang Liou

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
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  6. Article
  7. Biofilm and Cancer: Interactions and Future Directions for Cancer Therapy.International journal of molecular sciences · 2023
    Review
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  14. Experimental Study of Somatic Variants of Osteosarcoma by Whole-Exome Sequencing.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  15. 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

5 authors at 3 institutions in 1 country.

Yi-Ju WuInstitute of Cellular and System Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan 350, Taiwan. kathy614@nhri.org.tw.
Yee-Jee JanDepartment of Pathology and Laboratory Medicine, Taichung Veterans General Hospital, Taichung 407, Taiwan. yejan@vghtc.gov.tw.
Bor-Sheng KoDepartment of Internal Medicine, National Taiwan University Hospital, Taipei 100, Taiwan. kevinkomd@gmail.com.
Shu-Man LiangInstitute of Cellular and System Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan 350, Taiwan. shu-man@nhri.org.tw.
Jun-Yang LiouInstitute of Cellular and System Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan 350, Taiwan. jliou@nhri.org.tw.
National Health Research Institutes · TWNational Taiwan University Hospital · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There are seven mammalian isoforms of the 14-3-3 protein, which regulate multiple cellular functions via interactions with phosphorylated partners. Increased expression of 14-3-3 proteins contributes to tumor progression of various malignancies. Several isoforms of 14-3-3 are overexpressed and associate with higher metastatic risks and poorer survival rates of hepatocellular carcinoma (HCC). 14-3-3β and 14-3-3ζ regulate HCC cell proliferation, tumor growth and chemosensitivity via modulating mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK) and p38 signal pathways. Moreover, 14-3-3ε suppresses E-cadherin and induces focal adhesion kinase (FAK) expression, thereby enhancing epithelial-mesenchymal transition (EMT) and HCC cell migration. 14-3-3ζ forms complexes with αB-crystallin, which induces EMT and is the cause of sorafenib resistance in HCC. Finally, a recent study has indicated that 14-3-3σ induces heat shock protein 70 (HSP70) expression, which increases HCC cell migration. These results suggest that selective 14-3-3 isoforms contribute to cell proliferation, EMT and cell migration of HCC by regulating distinct targets and signal pathways. Targeting 14-3-3 proteins together with specific downstream effectors therefore has potential to be therapeutic and prognostic factors of HCC. In this article, we will overview 14-3-3's regulation of its downstream factors and contributions to HCC EMT, cell migration and proliferation.

Indexed as

14-3-3apoptosisepithelial-mesenchymal transitionhepatocellular carcinomamigrationproliferation

Identifiers

PMID26083935
PMCPMC4491697
OpenAlexW1581920763

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.