Evidence map›Paper›PMID 28154173›Full record

ArticleThe Journal of biological chemistry2017

Autocrine and Paracrine Interactions between Multiple Myeloma Cells and Bone Marrow Stromal Cells by Growth Arrest-specific Gene 6 Cross-talk with Interleukin-6.

Miki Furukawa, Hiroshi Ohkawara, Kazuei Ogawa, Kazuhiko Ikeda, Koki Ueda, Akiko Shichishima-Nakamura, Emi Ito, Jun-Ichi Imai, Yuka Yanagisawa, Reiko Honma and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. The Role of TAM Receptors in Bone.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. A 3D-Bioprinted Multiple Myeloma Model.Advanced healthcare materials · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

14 authors at 2 institutions in 4 countries.

Miki FurukawaFrom the Departments of Hematology.
Hiroshi OhkawaraFrom the Departments of Hematology, ohkawara@fmu.ac.jp.
Kazuei OgawaFrom the Departments of Hematology.
Kazuhiko IkedaFrom the Departments of Hematology.
Koki UedaFrom the Departments of Hematology.
Akiko Shichishima-NakamuraFrom the Departments of Hematology.
Emi Itothe Translational Research Center, Fukushima Medical University, Fukushima 960-1295 and.
Jun-Ichi Imaithe Translational Research Center, Fukushima Medical University, Fukushima 960-1295 and.
Yuka Yanagisawathe Translational Research Center, Fukushima Medical University, Fukushima 960-1295 and.
Reiko HonmaNIPPON GENE Co., Ltd., Tokyo 101-0054 Japan.
Shinya Watanabethe Translational Research Center, Fukushima Medical University, Fukushima 960-1295 and.
Satoshi Wagurithe Translational Research Center, Fukushima Medical University, Fukushima 960-1295 and.
Takayuki IkezoeFrom the Departments of Hematology.
Yasuchika TakeishiCardiovascular Medicine and.
Fukushima Medical University · JPNational Blood Transfusion Service · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of multiple myeloma (MM) has not yet been fully elucidated. Our microarray analysis and immunohistochemistry revealed significant up-regulation of growth arrest-specific gene 6 (Gas6), a vitamin K-dependent protein with a structural homology with protein S, in bone marrow (BM) cells of MM patients. ELISA showed that the serum levels of soluble Gas6 were significantly increased in the MM patients when compared with healthy controls. Gas6 was overexpressed in the human CD138-positive MM cell line RPMI-8226. Exogenous Gas6 suppressed apoptosis induced by serum deprivation and enhanced cell proliferation of the MM cells. The conditional medium from the human BM stromal cell line HS-5 induced cell proliferation and anti-apoptosis of the MM cells with extracellular signal-regulated kinase, Akt, and nuclear factor-κB phosphorylation, which were reversed by the neutralizing antibody to Gas6 or IL-6. The TAM family receptor Mer, which has been identified as a Gas6 receptor, was overexpressed in BM cells of MM patients. The knockdown of Mer by siRNA inhibited cell proliferation, anti-apoptosis, and up-regulation of intercellular cell adhesion molecule-1 (ICAM-1) in MM cells stimulated by an HS-5 cell-conditioned medium. Furthermore, the Gas6-neutralizing antibody reduced the up-regulation of IL-6 and ICAM-1 induced by a HS-5 cell-conditioned medium in MM cells. The present study provides new evidence that autocrine and paracrine stimulation of Gas6 in concert with IL-6 contributes to the pathogenesis of MM, suggesting that Gas6-Mer-related signaling pathways may be a promising novel target for treating MM.

Indexed as

Autocrine CommunicationCell ProliferationGrowth Arrest-Specific Protein 6HumansIntercellular Signaling Peptides and ProteinsInterleukin-6Mesenchymal Stem CellsMultiple MyelomaNF-kappa BParacrine CommunicationPhosphorylationSignal TransductionTumor Cells, CulturedGrowth Arrest-Specific Protein 6IL6 protein, humanIntercellular Signaling Peptides and ProteinsInterleukin-6NF-kappa Bapoptosisbone marrowcell proliferationinterleukin 6 (IL-6)multiple myelomastromal cell

Identifiers

PMID28154173
PMCPMC5354500
OpenAlexW2585858009

What OpenQuestion holds

Textmetadata
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.