Evidence map›Paper›PMID 40204967›Full record

ArticleScientific reports2025

Transcriptional regulation of ETV5 by mitogen-activated protein kinase via ETS-1 in human pancreatic cancer cells.

Aya Noguchi, Masanobu Kimura, Yuriko Saiki, Tomohiko Ishikawa, Takashi Kokumai, Yuko Omori, Yusuke Ono, Yusuke Miszukami, Masaharu Ishida, Masamichi Mizuma and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Aya NoguchiDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryomachi, Aobaku, Sendai, 980-8575, Japan.
Masanobu KimuraDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryomachi, Aobaku, Sendai, 980-8575, Japan.
Yuriko SaikiDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryomachi, Aobaku, Sendai, 980-8575, Japan.
Tomohiko IshikawaDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryomachi, Aobaku, Sendai, 980-8575, Japan.
Takashi KokumaiDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, 980-8574, Japan.
Yuko OmoriDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryomachi, Aobaku, Sendai, 980-8575, Japan.
Yusuke OnoInstitute of Biomedical Research, Sapporo Higashi Tokushukai Hospital, Sapporo, Japan.
Yusuke MiszukamiInstitute of Biomedical Research, Sapporo Higashi Tokushukai Hospital, Sapporo, Japan.
Masaharu IshidaDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, 980-8574, Japan.
Masamichi MizumaDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, 980-8574, Japan.
Kei NakagawaDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, 980-8574, Japan.
Michiaki UnnoDepartment of Surgery, Tohoku University Graduate School of Medicine, Sendai, 980-8574, Japan.
Toru FurukawaDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryomachi, Aobaku, Sendai, 980-8575, Japan. toru.furukawa.e2@tohoku.ac.jp.

Funding

Japan Society for the Promotion of Science JP23K24101
6 · The paper itself

Abstract

Pancreatic cancer is characterized by constitutive activation of mitogen-activated protein kinase /extracellular signal-regulated kinase 1/2 (ERK1/2) driven by gain-of-function mutations of KRAS. Our previous transcriptome sequencing of ERK1/2-attenuated cultured pancreatic cancer cells unveiled numerous downstream genes activated by ERK1/2 including ETV5. In this study, we explored the mechanism of transcriptional regulation of ETV5 by ERK1/2 in human pancreatic cancer cells. Detailed reporter assays uncovered a core promoter region spanning between - 350 and - 985 from the transcription start site of ETV5 as a strong responsive element to ERK1/2 activity. Moreover, ETS proto-oncogene 1, transcription factor (ETS-1) was found to bind to one of consensus binding sites in the core region and to promote ERK1/2-mediated upregulation of ETV5. Investigation of functional significances of ETS variant transcription factor 5 (ETV5) expression in the pancreatic cancer cells revealed that ETV5 was associated with resistance to gemcitabine; while no significance in proliferation, migration, and invasion. ETV5 expression in pancreatic ductal adenocarcinoma tissues resected from patients undergoing neoadjuvant chemotherapy was associated with KRAS mutations, which was consistent with ETV5 as a downstream upregulated molecule of RAS-ERK1/2 pathway. This study elucidated the mechanism of ERK1/2-mediated transcriptional regulation of ETV5 in human cancer cells, which could contribute to understand pancreatic cancer pathobiology.

Indexed as

DNA-Binding ProteinsGene Expression Regulation, NeoplasticPancreatic NeoplasmsProto-Oncogene Protein c-ets-1Transcription FactorsCell Line, TumorCell MovementCell ProliferationDeoxycytidineHumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 3Promoter Regions, GeneticProto-Oncogene MasTranscription, GeneticDeoxycytidineDNA-Binding ProteinsETS1 protein, humanETV5 protein, humanMAS1 protein, humanMitogen-Activated Protein Kinase 3Proto-Oncogene MasProto-Oncogene Protein c-ets-1Transcription Factors

Identifiers

PMID40204967
PMCPMC11982384

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.