Evidence map›Paper›PMID 33221995›Full record

ArticleJournal of cancer research and clinical oncology2021

The forkhead box M1 (FOXM1) expression and antitumor effect of FOXM1 inhibition in malignant rhabdoid tumor.

Yuichi Shibui, Kenichi Kohashi, Akihiko Tamaki, Izumi Kinoshita, Yuichi Yamada, Hidetaka Yamamoto, Tomoaki Taguchi, Yoshinao Oda

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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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 1 institution in 1 country.

Yuichi ShibuiDepartment of Anatomic Pathology Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Kenichi KohashiDepartment of Anatomic Pathology Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Akihiko TamakiDepartment of Anatomic Pathology Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Izumi KinoshitaDepartment of Anatomic Pathology Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Yuichi YamadaDepartment of Anatomic Pathology Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Hidetaka YamamotoDepartment of Anatomic Pathology Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Tomoaki TaguchiDepartment of Pediatric Surgery, Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.
Yoshinao OdaDepartment of Anatomic Pathology Graduate School of Medical Sciences, Kyushu University, Maidashi3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan. oda@surgpath.med.kyushu-u.ac.jp.ORCID http://orcid.org/0000-0001-9636-1182
Kyushu University · JP

Funding

Japan Society for the Promotion of Science JP19H03444
6 · The paper itself

Abstract

purposeMalignant rhabdoid tumor (MRT) is a rare, highly aggressive sarcoma with an uncertain cell of origin. Despite the existing standard of intensive multimodal therapy, the prognosis of patients with MRT is very poor. Novel antitumor agents are needed for MRT patients. Forkhead box transcription factor 1 (FOXM1) is overexpressed and is correlated with the pathogenesis in several human malignancies. In this study, we identified the clinicopathological and prognostic values of the expression of FOXM1 and its roles in the progression of MRT.

methodsWe investigated the FOXM1 expression levels and their clinical significance in 23 MRT specimens using immunohistochemistry and performed clinicopathologic and prognostic analyses. We also demonstrated correlations between the downregulation of FOXM1 and oncological characteristics using small interfering RNA (siRNA) and FOXM1 inhibitor in MRT cell lines.

resultsHistopathological analyses revealed that primary renal MRTs showed significantly low FOXM1 protein expression levels (p = 0.032); however, there were no significant differences in other clinicopathological characteristics or the survival rate. FOXM1 siRNA and FOXM1 inhibitor (thiostrepton) successfully downregulated the mRNA and protein expression of FOXM1 in vitro and the downregulation of FOXM1 inhibited cell proliferation, drug resistance to chemotherapeutic agents, migration, invasion, and caused the cell cycle arrest and apoptosis of MRT cell lines. A cDNA microarray analysis showed that FOXM1 regulated FANCD2 and NBS1, which are key genes for DNA damage repair.

conclusionThis study demonstrates that FOXM1 may serve as a promising therapeutic target for MRT.

Indexed as

Antineoplastic AgentsApoptosisCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDNA DamageDown-RegulationFanconi Anemia Complementation Group D2 ProteinFemaleForkhead Box Protein M1Gene Expression Regulation, NeoplasticHumansImmunohistochemistryInfantMaleAntineoplastic AgentsFanconi Anemia Complementation Group D2 ProteinForkhead Box Protein M1FOXM1 protein, humanNuclear ProteinsRNA, MessengerRNA, Small InterferingThiostreptonCell cycleFANCD2FOXM1Malignant rhabdoid tumorNBS1

Identifiers

PMID33221995
PMCPMC11801964
OpenAlexW3110230507

What OpenQuestion holds

Textmetadata
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.