Evidence map›Paper›PMID 25826092›Full record

ArticleOncotarget2015

Leucine-rich α-2-glycoprotein promotes TGFβ1-mediated growth suppression in the Lewis lung carcinoma cell lines.

Norihiko Takemoto, Satoshi Serada, Minoru Fujimoto, Hiromi Honda, Tomoharu Ohkawara, Tsuyoshi Takahashi, Shintaro Nomura, Hidenori Inohara, Tetsuji Naka

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
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  7. Article
  8. LRG1: an emerging player in disease pathogenesis.Journal of biomedical science · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Paradoxical Roles of Leucine-Rich αFrontiers in cell and developmental biology · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Leucine-richPhysiological reports · 2017
    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

9 authors at 3 institutions in 1 country.

Norihiko TakemotoDepartment of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Ibaraki, Osaka, Japan.
Satoshi SeradaLaboratory of Immune Signal, National Institute of Biomedical Innovation, Ibaraki, Osaka, Japan.
Minoru FujimotoLaboratory of Immune Signal, National Institute of Biomedical Innovation, Ibaraki, Osaka, Japan.
Hiromi HondaLaboratory of Immune Signal, National Institute of Biomedical Innovation, Ibaraki, Osaka, Japan.
Tomoharu OhkawaraLaboratory of Immune Signal, National Institute of Biomedical Innovation, Ibaraki, Osaka, Japan.
Tsuyoshi TakahashiLaboratory of Immune Signal, National Institute of Biomedical Innovation, Ibaraki, Osaka, Japan.
Shintaro NomuraDepartment of Animal Bioscience, Nagahama Institute of Bio-Science and Technology, Ibaraki, Osaka, Japan.
Hidenori InoharaDepartment of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Ibaraki, Osaka, Japan.
Tetsuji NakaLaboratory of Immune Signal, National Institute of Biomedical Innovation, Ibaraki, Osaka, Japan.
National Institute of Biomedical Innovation, Health and Nutrition · JPOsaka University · JPNagahama Institute of Bio-Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leucine-rich α2-glycoprotein (LRG) is an approximately 50-kDa glycoprotein that has been found to be elevated in the sera of patients with several types of cancer. LRG directly binds to transforming growth factor beta 1 (TGFβ1) and modulates TGFβ1 signaling in endothelial cells; however, the precise function of LRG in cancer remains unclear. This study aimed to investigate the role of LRG in cancer. Lewis lung carcinoma (LLC) cells hardly expressed LRG. The growth of LLC tumors allografted in the LRG knockout (KO) mice was significantly increased compared with wild-type (WT) mice. Conversely, overexpression of LRG significantly inhibited the growth of LLC tumors in WT mice. In the presence of LRG, TGFβ1 significantly inhibited the proliferation of LLC cells and human hepatocellular carcinoma Hep3B cells in vitro by inducing apoptosis via the potent activation of smad2 and its downstream signaling pathway. Furthermore, administration of a TGFβR1 inhibitor (SB431542) significantly enhanced the growth of LLC tumors in WT mice compared with LRG KO mice via inhibition of apoptosis. We propose that LRG potentiates the effect of TGFβ1 in cancer cells whose growth is suppressed in the presence of TGFβ1.

Indexed as

ApoptosisAnimalsBlotting, WesternCarcinoma, HepatocellularCarcinoma, Lewis LungCell ProliferationFemaleGlycoproteinsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutReal-Time Polymerase Chain ReactionGlycoproteinsLRG1 protein, mouseRNA, MessengerTransforming Growth Factor beta1apoptosisleucine-rich α-2-glycoproteinLewis lung carcinomasmad signal transductionTGFβ

Identifiers

PMID25826092
PMCPMC4484435
OpenAlexW1957520469

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.