Evidence map›Paper›PMID 38622340›Full record

ArticleCancer gene therapy2024

Inhibition of the galactosyltransferase C1GALT1 reduces osteosarcoma cell proliferation by interfering with ERK signaling and cell cycle progression.

Kentaro Watanabe, Keiji Tasaka, Hideto Ogata, Shota Kato, Hiroo Ueno, Katsutsugu Umeda, Tomoya Isobe, Yasuo Kubota, Masahiro Sekiguchi, Shunsuke Kimura and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

18 authors at 4 institutions in 1 country.

Kentaro WatanabeDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-0868-5289
Keiji TasakaDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hideto OgataDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shota KatoDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hiroo UenoDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Katsutsugu UmedaDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-6844-2011
Tomoya IsobeDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-3487-3307
Yasuo KubotaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-7909-5422
Masahiro SekiguchiDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-7941-9319
Shunsuke KimuraDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-2158-467X
Aiko Sato-OtsuboDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-2528-0702
Mitsuteru HiwatariDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-3683-4472
Tetsuo UshikuDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Motohiro KatoDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Akira OkaDepartment of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Satoru MiyanoDepartment of Integrated Analytics, M&D Data Science Center, Tokyo Medical and Dental University, Tokyo, Japan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Junko TakitaDepartment of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan. jtakita@kuhp.kyoto-u.ac.jp.ORCID 0000-0002-2452-6520
The University of Tokyo · JPKyoto University · JPHiroshima University · JPTokyo Medical and Dental University · JP

Funding

Japan Agency for Medical Research and Development (AMED) 23ama221505h0002Japan Agency for Medical Research and Development (AMED) JP22cm0106xxxh000x
6 · The paper itself

Abstract

Novel therapeutic strategies are urgently required for osteosarcoma, given the early age at onset and persistently high mortality rate. Modern transcriptomics techniques can identify differentially expressed genes (DEGs) that may serve as biomarkers and therapeutic targets, so we screened for DEGs in osteosarcoma. We found that osteosarcoma cases could be divided into fair and poor survival groups based on gene expression profiles. Among the genes upregulated in the poor survival group, siRNA-mediated knockdown of the glycosylation-related gene C1GALT1 suppressed osteosarcoma cell proliferation in culture. Gene expression, phosphorylation, and glycome array analyses also demonstrated that C1GALT1 is required to maintain ERK signaling and cell cycle progression. Moreover, the C1GALT1 inhibitor itraconazole suppressed osteosarcoma cell proliferation in culture, while doxycycline-induced shRNA-mediated knockdown reduced xenograft osteosarcoma growth in mice. Elevated C1GALT1 expression is a potential early predictor of poor prognosis, while pharmacological inhibition may be a feasible treatment strategy for osteosarcoma.

Indexed as

Cell CycleCell ProliferationGalactosyltransferasesMAP Kinase Signaling SystemOsteosarcomaAnimalsBone NeoplasmsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeXenograft Model Antitumor AssaysC1GALT1 protein, humanGalactosyltransferases

Identifiers

PMID38622340
PMCPMC11257960
OpenAlexW4394818532

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.