Evidence map›Paper›PMID 35085258›Full record

ArticlePloS one

Nicotine treatment regulates PD-L1 and PD-L2 expression via inhibition of Akt pathway in HER2-type breast cancer cells.

Masanori A Murayama, Erika Takada, Kenji Takai, Nagisa Arimitsu, Jun Shimizu, Tomoko Suzuki, Noboru Suzuki

Open access · goldAbstract read
In one paragraph

Article in PloS one. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

7 authors at 2 institutions in 1 country.

Masanori A MurayamaDepartment of Immunology and Medicine, St. Marianna University of School of Medicine, Miyamae-ku, Kawasaki, Kanagawa, Japan.ORCID https://orcid.org/0000-0002-0049-0316
Erika TakadaDepartment of Immunology and Medicine, St. Marianna University of School of Medicine, Miyamae-ku, Kawasaki, Kanagawa, Japan.
Kenji TakaiDepartment of Immunology and Medicine, St. Marianna University of School of Medicine, Miyamae-ku, Kawasaki, Kanagawa, Japan.
Nagisa ArimitsuDepartment of Immunology and Medicine, St. Marianna University of School of Medicine, Miyamae-ku, Kawasaki, Kanagawa, Japan.
Jun ShimizuDepartment of Immunology and Medicine, St. Marianna University of School of Medicine, Miyamae-ku, Kawasaki, Kanagawa, Japan.
Tomoko SuzukiDepartment of Immunology and Medicine, St. Marianna University of School of Medicine, Miyamae-ku, Kawasaki, Kanagawa, Japan.
Noboru SuzukiDepartment of Immunology and Medicine, St. Marianna University of School of Medicine, Miyamae-ku, Kawasaki, Kanagawa, Japan.ORCID https://orcid.org/0000-0001-7090-7415
St. Marianna University School of Medicine · JPKansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune checkpoint molecules such as PD-L1 and PD-L2 have a substantial contribution to cancer immunotherapy including breast cancer. Microarray expression profiling identified several molecular subtypes, namely luminal-type (with a good-prognosis), HER2-type (with an intermediate-prognosis), and triple-negative breast cancer (TNBC)-type (with a poor-prognosis). We found that PD-L1 and PD-L2 mRNA expressions were highly expressed in TNBC-type cell lines (HCC1937, MDA-MB-231), moderately expressed in HER2-type cell line (SK-BR-3), and poorly expressed in luminal-type cell lines (MDA-MB-361, MCF7). The PD-L1 and PD-L2 expression in SK-BR-3 cells, but not those in HCC1937 and MDA-MB-231 cells, decreased by nicotine stimulation in a dose-dependent manner. In addition, nicotine treatment decreased the phosphorylation of Akt in SK-BR-3 cells, but not in other cell lines. These results show that nicotine regulates the expression of immune checkpoint molecules, PD-L1 and PD-L2, via inhibition of Akt phosphorylation. This findings may provide the new therapeutic strategies for the treatment of breast cancer.

Indexed as

B7-H1 AntigenBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, DrugErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHumansNicotinePhosphorylationProgrammed Cell Death 1 Ligand 2 ProteinProto-Oncogene Proteins c-aktSignal TransductionUp-RegulationB7-H1 AntigenCD274 protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesNicotinePDCD1LG2 protein, humanProgrammed Cell Death 1 Ligand 2 ProteinProto-Oncogene Proteins c-akt

Identifiers

PMID35085258
PMCPMC8794171
OpenAlexW4210272200

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.