Evidence map›Paper›PMID 40318167›Full record

ArticleThe FEBS journal2025

Zic family member 5 promotes RIO kinase 3 expression to enhance pancreatic cancer survival.

Reiko Satow, Yuki Kashiwaba, Misaki Okao, Shin Takano, Yuna Aiga, Atsuko Yoneda, Kazuyoshi Hosomichi, Kiyoko Fukami

Abstract read
In one paragraph

Article in The FEBS journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Reiko SatowLaboratory of Computational Genomics, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.ORCID https://orcid.org/0000-0002-6339-4268
Yuki KashiwabaLaboratory of Computational Genomics, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.
Misaki OkaoLaboratory of Computational Genomics, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.
Shin TakanoLaboratory of Computational Genomics, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.
Yuna AigaLaboratory of Computational Genomics, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.
Atsuko YonedaLaboratory of Computational Genomics, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.
Kazuyoshi HosomichiLaboratory of Computational Genomics, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.
Kiyoko FukamiLaboratory of Genome and Biosignals, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Japan.

Funding

Japan Society for the Promotion of Science 26860221Princess Takamatsu Cancer Research Fund
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies with few effective therapies available. We previously determined the essential role of Zic family member 5 (ZIC5) in the survival of PDAC cells. In this study, we showed that targeting ZIC5 can effectively shrink PDAC tumors treated with gemcitabine in vivo and investigated the molecular mechanisms involved. When tumor-bearing mice were injected intravenously with ZIC5-targeting small interfering RNA, tumor volume was significantly reduced by gemcitabine treatment. RNA-sequencing analysis was used to identify the genes affected by ZIC5 knockdown. Among these, we selected the genes whose mRNA expression levels correlated with that of ZIC5 in pancreatic cancer and those associated with poor prognosis in patients with pancreatic cancer. Further analysis revealed that RIO kinase 3 (RIOK3) promotes PDAC cell survival, whereas ALDH3B1, PTGES, and TUFT1 contribute to gemcitabine resistance in MiaPaca-2 cells. We identified RIOK3 as a direct target gene of ZIC5 using ChIP and luciferase assays. Furthermore, stable expression of RIOK3 in PANC-1 cells reversed the reduction in cell number following ZIC5 knockdown. These findings highlight RIOK3 as a critical target of ZIC5, which is involved in survival signaling in PDAC cells.

Indexed as

Carcinoma, Pancreatic DuctalDNA-Binding ProteinsPancreatic NeoplasmsProtein Serine-Threonine KinasesTranscription FactorsAnimalsCell Line, TumorCell SurvivalDeoxycytidineDrug Resistance, NeoplasmGemcitabineGene Expression Regulation, NeoplasticHumansMiceMice, NudeXenograft Model Antitumor AssaysDeoxycytidineDNA-Binding ProteinsGemcitabineProtein Serine-Threonine KinasesTranscription Factorscancer survivaldrug resistancegemcitabine sensitivitypancreatic ductal adenocarcinoma

Identifiers

PMID40318167
PMCPMC12326931

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Registered trials

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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.