Evidence map›Paper›PMID 41482357›Full record

ArticleCancer genomics & proteomics

DNA Damage-induced Post-transcriptional Regulation of SIRT4 by the miR-15/16 Family Modulates Chemosensitivity in Cancer Cells.

Sangyeon Won, Minbeom Ko, Seung Min Jeong

Abstract read
In one paragraph

Article in Cancer genomics & proteomics. 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

3 authors.

Sangyeon Won *Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Minbeom Ko *Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Seung Min JeongDepartment of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea; smjeong@catholic.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimSIRT4 is a mitochondrial regulator of metabolism and stress responses, yet the mechanisms underlying its induction upon DNA damage remains unclear. This study aimed to define the mechanism of SIRT4 regulation and the role of the miR-15/16 family in this process. MATERIALS AND

methodsSIRT4 expression was examined after DNA-damaging treatments in MEFs and HeLa cells. Reporter assays, mRNA decay analysis, and mutagenesis of the SIRT4 3'UTR were performed to identify regulatory mechanisms. Gain- and loss-of-function studies assessed the involvement of the miR-15/16 family. Cell viability was evaluated.

resultsSIRT4 was strongly induced by DNA damage and required for cell survival under genotoxic stress. This induction occurred through mRNA stabilization with the 3'UTR of SIRT4 serving as the determinant of stability. The miR-15/16 family targeted a conserved site within the SIRT4 3'UTR to destabilize its mRNA. Overexpression of miR-15/16 reduced SIRT4 expression and sensitized cells to chemotherapy.

conclusionThe miR-15/16-SIRT4 axis represents a novel mechanism of post-transcriptional regulation in the DNA damage response and may serve as a therapeutic target to improve the efficacy of chemotherapy.

Indexed as

DNA DamageDrug Resistance, NeoplasmMicroRNAsMitochondrial ProteinsNeoplasmsSirtuins3' Untranslated RegionsAnimalsGene Expression Regulation, NeoplasticHeLa CellsHumansMice3' Untranslated RegionsMicroRNAsMIRN15 microRNA, humanMIRN16 microRNA, humanMitochondrial ProteinsSIRT4 protein, humanSirtuinschemosensitivityDNA damagemiR-15/16 familymRNA stabilitySIRT4

Identifiers

PMID41482357
PMCPMC12758664

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.