Evidence map›Paper›PMID 41786918›Full record

ArticleScientific reports2026

Caffeic acid suppresses cyclin D1 expression by directly binding to ribosomal protein S5 in colorectal cancer cells.

Motoki Watanabe, Shogen Boku, Mamiko Sukeno, Kaito Kobayashi, Tomoshi Kameda, Yosuke Iizumi, Wataru Nishio, Michihiro Mutoh, Toshiyuki Sakai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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.

Motoki WatanabeDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan. mtkw@koto.kpu-m.ac.jp.
Shogen BokuDepartment of Clinical Oncology, Kansai Medical University Hospital, Osaka, Japan.
Mamiko SukenoDepartment of Drug Discovery Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kaito KobayashiArtificial Intelligence Research Center, National Institute of Advanced Industrial Science and Technology (AIST), Tokyo, Japan.
Tomoshi KamedaArtificial Intelligence Research Center, National Institute of Advanced Industrial Science and Technology (AIST), Tokyo, Japan.
Yosuke IizumiDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Wataru NishioDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Michihiro MutohDepartment of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Toshiyuki SakaiDepartment of Drug Discovery Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Funding

Japan Society for the Promotion of Science Grant in Aid for Early-Career Scientists (18K17355)Kyoto Preventive Medical Center Cancer Grant in Aid (5-050)
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, and dietary components such as coffee have been epidemiologically associated with a reduced risk of CRC. However, the molecular mechanisms underlying this effect remain elusive. In this study, we found that caffeic acid, a hydrolysate of chlorogenic acid abundant in coffee, significantly suppressed colony formation in human CRC cells. Chemical pull-down assays using nano-magnetic beads combined with mass spectrometry identified ribosomal protein S5 (RPS5) as a direct binding target of caffeic acid. Molecular dynamics simulations further supported the stability of the interaction between caffeic acid and a specific binding pocket on RPS5. Mechanistically, RNA interference-mediated knockdown of RPS5 induced G1 cell cycle arrest and downregulated cyclin D1 expression at both mRNA and protein levels, without affecting its promoter activity, suggesting a post-transcriptional regulatory mechanism of cyclin D1 by RPS5. These findings reveal a previously unrecognized RPS5-cyclin D1 axis targeted by caffeic acid and provide novel mechanistic insights into the potential chemopreventive effects of coffee against CRC.

Indexed as

Caffeic AcidsColorectal NeoplasmsCyclin D1Gene Expression Regulation, NeoplasticRibosomal ProteinsCell Line, TumorCell ProliferationG1 Phase Cell Cycle CheckpointsHumansMolecular Dynamics SimulationProtein Bindingcaffeic acidCaffeic AcidsCCND1 protein, humanCyclin D1Ribosomal ProteinsCaffeic acidColorectal cancerCyclin D1RPS5

Identifiers

PMID41786918
PMCPMC13096365

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.