Evidence map›Paper›PMID 26391953›Full record

ArticleMolecular and cellular biology2015

Regulation of the Mechanism of TWIST1 Transcription by BHLHE40 and BHLHE41 in Cancer Cells.

Kazuo Asanoma, Ge Liu, Takako Yamane, Yoko Miyanari, Tomoka Takao, Hiroshi Yagi, Tatsuhiro Ohgami, Akimasa Ichinoe, Kenzo Sonoda, Norio Wake and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.1field-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

36 citing papers in PubMed, 48 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Kazuo AsanomaDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan asanoma@med.kyushu-u.ac.jp.
Ge LiuResearch Center for Environment and Developmental Medical Sciences, Kyushu University, Fukuoka, Japan.
Takako YamaneDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Yoko MiyanariDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tomoka TakaoCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University, Kyoto, Japan.
Hiroshi YagiDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tatsuhiro OhgamiDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Akimasa IchinoeDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kenzo SonodaDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Norio WakeResearch Center for Environment and Developmental Medical Sciences, Kyushu University, Fukuoka, Japan.
Kiyoko KatoDepartment of Obstetrics and Gynecology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kyushu University · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BHLHE40 and BHLHE41 (BHLHE40/41) are basic helix-loop-helix type transcription factors that play key roles in multiple cell behaviors. BHLHE40/41 were recently shown to be involved in an epithelial-to-mesenchymal transition (EMT). However, the precise mechanism of EMT control by BHLHE40/41 remains unclear. In the present study, we demonstrated that BHLHE40/41 expression was controlled in a pathological stage-dependent manner in human endometrial cancer (HEC). Our in vitro assays showed that BHLHE40/41 suppressed tumor cell invasion. BHLHE40/41 also suppressed the transcription of the EMT effectors SNAI1, SNAI2, and TWIST1. We identified the critical promoter regions of TWIST1 for its basal transcriptional activity. We elucidated that the transcription factor SP1 was involved in the basal transcriptional activity of TWIST1 and that BHLHE40/41 competed with SP1 for DNA binding to regulate gene transcription. This study is the first to report the detailed functions of BHLHE40 and BHLHE41 in the suppression of EMT effectors in vitro. Our results suggest that BHLHE40/41 suppress tumor cell invasion by inhibiting EMT in tumor cells. We propose that BHLHE40/41 are promising markers to predict the aggressiveness of each HEC case and that molecular targeting strategies involving BHLHE40/41 and SP1 may effectively regulate HEC progression.

Indexed as

Basic Helix-Loop-Helix ProteinsBinding SitesBiomarkers, TumorCell Line, TumorDisease ProgressionDNA-Binding ProteinsEndometrial NeoplasmsEpithelial-Mesenchymal TransitionFemaleHEK293 CellsHomeodomain ProteinsHumansNeoplasm InvasivenessNuclear ProteinsPromoter Regions, GeneticRNA InterferenceBasic Helix-Loop-Helix ProteinsBHLHE40 protein, humanBHLHE41 protein, humanBiomarkers, TumorDNA-Binding ProteinsHomeodomain ProteinsNuclear ProteinsRNA, MessengerRNA, Small InterferingSNAI1 protein, humanSNAI2 protein, humanSnail Family Transcription FactorsSP1 protein, humanSp1 Transcription FactorTranscription FactorsTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID26391953
PMCPMC4648814
OpenAlexW2177908652

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.