Evidence map›Paper›PMID 31601917›Full record

ArticleScientific reports2019

A novel therapeutic approach for anaplastic thyroid cancer through inhibition of LAT1.

Keisuke Enomoto, Fuyuki Sato, Shunji Tamagawa, Mehmet Gunduz, Naoyoshi Onoda, Shinya Uchino, Yasuteru Muragaki, Muneki Hotomi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024
    Review
  13. Article
  14. Small molecule inhibitors for cancer metabolism: promising prospects to be explored.Journal of cancer research and clinical oncology · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 3 institutions in 1 country.

Keisuke EnomotoDepartments of Otolaryngology-Head and Neck Surgery, Wakayama Medical University, Wakayama, Japan.
Fuyuki SatoDepartments of Pathology, Wakayama Medical University, Wakayama, Japan.
Shunji TamagawaDepartments of Otolaryngology-Head and Neck Surgery, Wakayama Medical University, Wakayama, Japan.
Mehmet GunduzDepartments of Otolaryngology-Head and Neck Surgery, Wakayama Medical University, Wakayama, Japan.
Naoyoshi OnodaDepartment of Breast & Endocrine Surgery, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Shinya UchinoNoguchi Thyroid Clinic and Hospital Foundation, Oita, Japan.
Yasuteru MuragakiDepartments of Pathology, Wakayama Medical University, Wakayama, Japan.
Muneki HotomiDepartments of Otolaryngology-Head and Neck Surgery, Wakayama Medical University, Wakayama, Japan. mhotomi@wakayama-med.ac.jp.
Wakayama Medical University · JPNoguchi Thyroid Clinic and Hospital Foundation · JPOsaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A novel therapeutic approach is urgently needed for patients with anaplastic thyroid cancer (ATC) due to its fatal and rapid progress. We recently reported that ATC highly expressed MYC protein and blocking of MYC through its selective inhibitor, JQ1, decreased ATC growth and improved survival in preclinical models. One of the important roles of MYC is regulation of L-neutral amino acid transporter 1 (LAT1) protein and inhibition of LAT1 would provide similar anti-tumor effect. We first identified that while the human ATC expresses LAT1 protein, it is little or not detected in non-cancerous thyroidal tissue, further supporting LAT1 as a good target. Then we evaluated the efficacy of JPH203, a LAT1 inhibitor, against ATC by using the in vitro cell-based studies and in vivo xenograft model bearing human ATC cells. JPH203 markedly inhibited proliferation of three ATC cell lines through suppression of mTOR signals and blocked cell cycle progression from the G0/G1 phase to the S phase. The tumor growth inhibition and decrease in size by JPH203 via inhibition of mTOR signaling and G0/G1 cell cycle associated proteins were further confirmed in xenograft models. These preclinical findings suggest that LAT1 inhibitors are strong candidates to control ATC, for which current treatment options are highly limited.

Indexed as

AnimalsAntineoplastic AgentsBenzoxazolesCell Line, TumorCell ProliferationFemaleG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansLarge Neutral Amino Acid-Transporter 1MiceMolecular Targeted TherapySignal TransductionThyroid Carcinoma, AnaplasticThyroid NeoplasmsTOR Serine-Threonine Kinases2-amino-3-(4-((5-amino-2-phenylbenzo(d)oxazol-7-yl)methoxy)-3,5-dichlorophenyl)propanoic acidAntineoplastic AgentsBenzoxazolesLarge Neutral Amino Acid-Transporter 1MTOR protein, humanSLC7A5 protein, humanTOR Serine-Threonine KinasesTyrosine

Identifiers

PMID31601917
PMCPMC6787004
OpenAlexW2979874806

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.