Evidence map›Paper›PMID 31014014›Full record

ReviewInternational journal of molecular sciences2019

C-X-C Motif Chemokine Ligand 14 is a Unique Multifunctional Regulator of Tumor Progression.

Xiao-Yan Yang, Shigeyuki Ozawa, Yasumasa Kato, Yojiro Maehata, Kazuhito Izukuri, Takeharu Ikoma, Keisuke Kanamori, Tetsu Akasaka, Kenji Suzuki, Hiroshi Iwabuchi and 5 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Exosomal CXCL14 Contributes to M2 Macrophage Polarization through NF-Oxidative medicine and cellular longevity · 2022
    Article
  12. Article
  13. Review
  14. 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

15 authors at 3 institutions in 1 country.

Xiao-Yan YangOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. yang@kdu.ac.jp.
Shigeyuki OzawaOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. ozawa@kdu.ac.jp.
Yasumasa KatoDepartment of Oral Function and Molecular Biology, Ohu University School of Dentistry, Koriyama 963-8611, Japan. y-katou@den.ohu-u.ac.jp.ORCID 0000-0003-0192-9324
Yojiro MaehataOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. maehata@kdu.ac.jp.
Kazuhito IzukuriOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. izukuri@kdu.ac.jp.
Takeharu IkomaOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. t.ikoma@kdu.ac.jp.
Keisuke KanamoriOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. mmafighter5050@gmail.com.
Tetsu AkasakaOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. akasaka@kdu.ac.jp.
Kenji SuzukiDepartment of Dentomaxillofacial Diagnosis and Treatment, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. k.suzuki@kdu.ac.jp.
Hiroshi IwabuchiDepartment of Dentomaxillofacial Diagnosis and Treatment, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. iwabuchi@kdu.ac.jp.
Shun-Ichi KurataOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. kurata@kdu.ac.jp.
Iyoko KatohOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. katoh.iyoko@kdu.ac.jp.
Takashi SakuraiDepartment of Dentomaxillofacial Diagnosis and Treatment, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. t.sakurai@kdu.ac.jp.
Tohru KiyonoDivision of Carcinogenesis and Cancer Prevention, Department of Cell Culture Technology, National Cancer Center Research Institute, Tokyo 104-0045, Japan. tkiyono@ncc.go.jp.
Ryu-Ichiro HataOral Health Science Research Center, Graduate School of Kanagawa Dental University, Yokosuka 238-8580, Japan. ryuhata@gmail.com.
Kanagawa Dental University · JPJapan Institute of Leather Research · JPOhu University · JP

Funding

Japan Society for the Promotion of Science 16K11707, 16K11736, 17K17112, and 18K09779
6 · The paper itself

Abstract

Cancer is a leading cause of death and disease worldwide, with a tremendous financial impact. Thus, the development of cost-effective novel approaches for suppressing tumor growth and progression is essential. In an attempt to identify the mechanisms responsible for tumor suppression, we screened for molecules downregulated in a cancer progression model and found that the chemokine CXCL14, also called BRAK, was the most significantly downregulated. Increasing the production of CXCL14 protein by transfecting tumor cells with a CXCL14 expression vector and transplanting the cells into the back skin of immunodeficient mice suppressed tumor cell growth compared with that of parental tumor cells, suggesting that CXCL14 suppressed tumor growth in vivo. However, some studies have reported that over-expression of CXCL14, especially in stromal cells, stimulated the progression of tumor formation. Transgenic mice expressing 10-fold more CXCL14 protein than wild-type C57BL/6 mice showed reduced rates of chemical carcinogenesis, transplanted tumor growth, and metastasis without apparent side effects. CXCL14 also acts as an antimicrobial molecule. In this review, we highlight recent studies involving the identification and characterization of CXCL14 in cancer progression and discuss the reasons for the context-dependent effects of CXCL14 on tumor formation.

Indexed as

Anti-Infective AgentsAntineoplastic Agents, ImmunologicalCandidaCetuximabChemokines, CXCGram-Positive BacteriaHumansMitogen-Activated Protein KinasesNeoplasmsAnti-Infective AgentsAntineoplastic Agents, ImmunologicalCetuximabChemokines, CXCMitogen-Activated Protein Kinasesantimicrobial functionC-X-C motif chemokine ligand 14molecular preventive medicinemultifunctional tumor suppressor

Identifiers

PMID31014014
PMCPMC6514660
OpenAlexW2939706540

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.