Evidence map›Paper›PMID 34440595›Full record

ArticleLife (Basel, Switzerland)2021

Sphingosine-1-Phosphate Induces ATP Release via Volume-Regulated Anion Channels in Breast Cell Lines.

Kishio Furuya, Hiroaki Hirata, Takeshi Kobayashi, Masahiro Sokabe

Open access · goldAbstract read
In one paragraph

Article in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
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 1 institution in 1 country.

Kishio FuruyaMechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0003-4714-8689
Hiroaki HirataMechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0002-2604-9158
Takeshi KobayashiDepartment Physiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000-0002-4372-5285
Masahiro SokabeMechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Nagoya University · JP

Funding

Collaboration research between Nagoya Univ and R-Pharm 2614Dj-02bJapan Society for the Promotion of Science 24590274 15K08174 18K06851
6 · The paper itself

Abstract

High interstitial level of ATP and its lysate adenosine in the cancer microenvironment are considered a halo mark of cancer. Adenosine acts as a strong immune suppressor. However, the source of ATP release is unclear. We clarified the release of ATP via volume-regulated anion channels (VRACs) in breast cell lines using an ATP luminescence imaging system. We detected a slowly rising diffuse pattern of ATP release that was only observed in undifferentiated cells, not in differentiated primary cultured cells. This was confirmed by suppression with DCPIB, a blocker of VRACs, and shRNA for LRRC8A, an indispensable subunit of VRACs. We herein demonstrated that the inflammatory mediator sphingosine-1-phosphate (S1P), which exists abundantly in the cancer microenvironment, induced a diffuse pattern of ATP release isovolumetrically. The response was dose-dependent and suppressed by the knock-down of LRRC8A. It was also suppressed by blockers of S1P receptor 1 and 2 (W146 and JTE013, respectively). RTqPCR demonstrated the prominent presence of S1PR1 and S1PR2 mRNAs. We discussed the roles of S1P-induced ATP release in the cancer microenvironment.

Indexed as

ATP imagingATP releasebreast cancer cellhypotonic stressJTE013LRRC8AS1Ptumor microenvironmentVRACsW146

Identifiers

PMID34440595
PMCPMC8401269
OpenAlexW3195599863

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.