Evidence map›Paper›PMID 40682103›Full record

ArticleCell communication and signaling : CCS2025

MIR4726

Fangfang Li, Xinyi Long, Sishi Tang, Jinhua Yan, Jing Liu, Yunfeng Fu

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 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

6 authors.

Fangfang LiDepartment of Hematology, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.ORCID https://orcid.org/0009-0007-2372-3251
Xinyi LongDepartment of Hematology, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Sishi TangDepartment of Hematology, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Jinhua YanDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, 410013, China.
Jing LiuDepartment of Hematology, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.ORCID https://orcid.org/0000-0001-9245-316X
Yunfeng FuDepartment of Blood Transfusion, The Third Xiangya Hospital of Central South University, Changsha, 410013, China. fuyunfeng@csu.edu.cn.ORCID https://orcid.org/0000-0002-1319-4938

Funding

"co-PI" project from The Third Xiangya Hospital of Central South University 202408National Natural Science Foundation of China 81870166Natural Science Foundation of Changsha City kq2502026Natural Science Foundation of Hunan Province 2025JJ50706
6 · The paper itself

Abstract

backgroundDespite many new drugs, multiple myeloma (MM) remains an incurable plasma cell malignancy, and drug resistance is a long-standing topic in this field. Characterized by efficient transcription without being limited by the double helix structure and promoter, extrachromosomal circular DNA (EccDNA) has been proven to be widely involved in cancer development and drug resistance.

methodsWe performed circle-seq and mRNA-seq on samples from three MM patients at the time of complete response and relapse to screen EccDNA candidate molecules. Outward PCR and Sanger sequencing were used to identify EccDNA molecules. RT‒qPCR and WB were performed to detect gene expression levels. Fluorescence in situ hybridization (FISH) was carried out to detect the deletion of chromosome 17p (del (17p)). Transmission electron microscopy (TEM) was conducted to observe autophagosomes. Luciferase reporter assays were performed to validate the binding of microRNAs to target genes. Cell viability assays and apoptosis assays were employed to assess drug resistance. Xenograft tumor mouse models were established for in vivo experiments. Immunohistochemistry (IHC) was used to detect protein expression levels.

resultsWe successfully identified an EccDNA molecule (EccDNA

conclusionsIn summary, our findings indicate that artificially synthesized MIR4726

Indexed as

AutophagyBortezomibDrug Resistance, NeoplasmMicroRNAsMultiple MyelomaRNA-Binding ProteinsAnimalsApoptosisCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceBortezomibMicroRNAsRNA-Binding ProteinsAutophagyBortezomibExtrachromosomal circular DNA (EccDNA)MIR4726-5pMultiple myelomaNKIRAS2NXF1

Identifiers

PMID40682103
PMCPMC12273429

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.