Evidence map›Paper›PMID 41403630›Full record

ArticleArchives of medical science : AMS2025

LncRNA NEAT1 contributes to multiple myeloma progression via upregulating ARPC5 by sponging miR-133a.

Fujue Wang, Piaorong Zeng, Zhongwei Lu, Xingxing Long, Cong Luo, Juan Zuo, Yixiong Cao, Feng Wen, Junjun Li, Zeyu Luo

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Archives of medical science : AMS, 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

10 authors.

Fujue WangDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Piaorong ZengDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Zhongwei LuDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Xingxing LongDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Cong LuoDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Juan ZuoDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Yixiong CaoDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Feng WenDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Junjun LiDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.
Zeyu LuoDepartment of Hematology, Hengyang Medical School, University of South China, The First Affiliated Hospital, Hengyang, Hunan Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) is confirmed to be involved in regulation of the multiple myeloma (MM) process. However, its underlying molecular mechanism deserves further investigation. Material and methods: Quantitative real-time PCR was used to examine NEAT1, microRNA (miR)-133a and actin-related protein 2/3 complex subunit 5 (ARPC5) expression. Cell proliferation and apoptosis were evaluated by cell counting kit 8 assay, soft-agar colony formation assay and flow cytometry. Dual-luciferase reporter assay was used to confirm the interaction between miR-133a and NEAT1 or ARPC5. The localization of NEAT1 and miR-133a in MM cells was determined by fluorescent Results: NEAT1 had increased expression in MM patients and cells. NEAT1 knockdown could repress MM cell proliferation and enhance apoptosis. NEAT1 could sponge miR-133a, and miR-133a could target ARPC5. MiR-133a was lowly expressed and ARPC5 was highly expressed in MM patients. MiR-133a inhibitor could abolish the suppressive effect of NEAT1 knockdown on MM cell growth, and these effects also could be reversed by ARPC5 silencing. Conclusions: Animal experiments showed that NEAT1 downregulation reduced MM tumor growth by regulating miR-133a/ARPC5 axis. NEAT1 facilitated MM progression through the regulation of miR-133a/ARPC5, which provided new evidence that NEAT1 was a potential therapeutic target for MM.

Indexed as

ARPC5miR-133amultiple myelomaNEAT1

Identifiers

PMID41403630
PMCPMC12703598

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