Evidence map›Paper›PMID 42317311›Full record

ReviewFrontiers in immunology2026

Post-transcriptional regulation of mRNA stability in pancreatic ductal adenocarcinoma.

Heyang Wang, Pan Liu, Juntaro Yamasaki, Tatsuhiko Harada, Tatsuya Sakaguchi, Tetsuya Takimoto, Hideyuki Saya, Osamu Nagano, Kazuhiro Fukumura

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. 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

9 authors.

Heyang WangDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.
Pan LiuDepartment of Pharmacy, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Juntaro YamasakiDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.
Tatsuhiko HaradaDepartment of Advanced Robotic and Endoscopic Surgery, Fujita Health University, Toyoake, Japan.
Tatsuya SakaguchiDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.
Tetsuya TakimotoDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.
Hideyuki SayaDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.
Osamu NaganoDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.
Kazuhiro FukumuraDivision of Gene Regulation, Oncology Innovation Center, Fujita Health University, Toyoake, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies and is characterized by pronounced phenotypic plasticity, metabolic adaptation, and therapeutic resistance within a dense and desmoplastic tumor microenvironment. Although transcriptional deregulation has been extensively investigated, post-transcriptional regulation, particularly the control of mRNA stability, has emerged as a critical and previously underexplored contributor to PDAC progression. RNA-binding proteins (RBPs), together with cis-regulatory RNA elements and epitranscriptomic modifications such as N6-methyladenosine (m6A), form interconnected regulatory networks that dynamically modulate mRNA turnover and thereby shape protein output in response to microenvironmental stress. By selectively stabilizing transcripts encoding epithelial-mesenchymal transition (EMT) regulators, metabolic enzymes, and stress-response factors, these networks promote reversible, non-genetic adaptation without requiring permanent genetic alterations. This regulatory flexibility supports invasion, therapeutic tolerance, and intratumoral heterogeneity under hypovascular and nutrient-limited conditions. Recent advances further suggest that targeting mRNA stability through small molecules and RNA-directed strategies may provide new therapeutic opportunities in PDAC. In this review, we summarize current insights into post-transcriptional mechanisms regulating mRNA stability in PDAC, highlight key knowledge gaps, and discuss their potential translational implications.

Indexed as

Carcinoma, Pancreatic DuctalGene Expression Regulation, NeoplasticPancreatic NeoplasmsRNA, MessengerRNA Processing, Post-TranscriptionalRNA StabilityAnimalsEpithelial-Mesenchymal TransitionEpitranscriptomeHumansMetabolic ReprogrammingRNA-Binding ProteinsTumor MicroenvironmentRNA-Binding ProteinsRNA, Messengerepithelial–mesenchymal transition (EMT)m6A epitranscriptomicsmetabolic reprogrammingmRNA stabilitypancreatic ductal adenocarcinoma (PDAC)phenotypic plasticitypost-transcriptional regulationRNA-binding proteins (RBPs)

Identifiers

PMID42317311
PMCPMC13272327

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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.