Evidence map›Paper›PMID 41204251›Full record

ArticleJournal of translational medicine2025

The impact of STAiR18 on multiple myeloma survival rates.

Yingmiao Wu, Haolin Wang, Ji Luo, Jiaoya Lin, Yajie Wu, Shuai Zheng, Yifei Gao, Jiao Chen, Feifei Che, Jianyou Shi and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 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. Review
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

11 authors.

Yingmiao Wu *Genetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Haolin Wang *Genetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Ji LuoGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Jiaoya LinDepartment of Clinical Laboratory Diagnosis, The Affiliated Hospital, Southwest Medical University, Luzhou, Sichuan, China.
Yajie WuGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Shuai ZhengGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Yifei GaoGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Jiao ChenDepartment of Hematology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Feifei CheDepartment of Hematology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Jianyou ShiDepartment of Pharmacy, Personalized Drug Therapy Key Laboratory of Sichuan Province, Sichuan Academy of Medical Sciences & Sichuan Provincial, People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China. shijianyoude@126.com.
Ling ZhongGenetic Diseases Key Laboratory of Sichuan Province, Department of Medical Genetics, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China. zhongling@med.uestc.edu.cn.ORCID 0000-0003-3551-9921

Funding

CAMS Innovation Fund for Medical Sciences (CIFMS) 2023-I2M-C&T-B-124Medicine-engineering Interdisciplinary Granted by UESTC ZYGX2021YGLH006Scientific Research Project of Cadre Health Care in Sichuan Province 2023-212Sichuan Science and Technology Program 2023NSFSC0538Special Research Project of Research Fund of Sichuan Anti Cancer Association (Qilu) 2022HX040
6 · The paper itself

Abstract

backgroundA subset of multiple myeloma (MM) patients exhibited worse survival and higher tumor burden. STAiR18 has been found to be highly expressed in MM cell lines. However, the precise mechanisms underlying the upstream and downstream regulation of STAiR18 have remained unclear.

methodsThe expression of STAiR18 and miR-451a in MM patients and cell lines was detected using quantitative reverse transcriptase PCR (qRT-PCR). ChIP-qPCR was performed to assess the enrichment of pSTAT3 at the STAiR18 promoter. The subcellular localization of STAiR18 was determined by FISH. The binding relationship between STAiR18 and miR-451a was predicted through bioinformatics analyses and validated using RNA pull down and dual-luciferase reporter assays. Cell proliferation was evaluated with CCK-8 assay, Edu assay, and flow cytometry. The expression levels of key proteins in the IL-6R/STAT3/JAK2 pathway, along with Cyclin D1 and apoptosis-related markers, were analyzed by Western blot. Cell cycle distribution and apoptosis rate were quantified by flow cytometry. The role of STAiR18 was also investigated in vivo using a xenograft tumor model, which was established by tail vein injection of MM cell lines into NOG mice.

resultsIn MM patients, STAiR18 expression was notably upregulated in myeloma cells from bone marrow, and positively correlated with clinical stage and worse outcome. Knockdown (KD) and overexpression (OE) of STAT3 affected the expression level of STAiR18, and pSTAT3 was significantly enriched in STAiR18's promoter. Knockdown of STAiR18 reduced the proliferation of MM cells in vitro and suppressed tumor growth in vivo. STAiR18 was predicted and confirmed to primarily localize in the cytoplasm. STAiR18 KD resulted in upregulation of miR-451a levels. The binding between STAiR18 and miR-451a (silencing IL-6R) was predicted and validated. Through KD and rescue experiments, we demonstrated that STAiR18 sponged miR-451a, and promoted myeloma cell proliferation via IL-6R/STAT3/JAK2 pathway.

conclusionsThe study revealed that STAiR18 competed with endogenous miR-451a, and formed a novel positive-feedback loop of IL-6R/STAT3/JAK2 to promote proliferation of MM. These findings suggest that STAiR18 represents a promising novel therapeutic strategy for MM treatment.

Indexed as

Multiple MyelomaAnimalsApoptosisCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansJanus Kinase 2MaleMiceMicroRNAsPromoter Regions, GeneticSignal TransductionSTAT3 Transcription FactorSurvival RateJanus Kinase 2MicroRNAsSTAT3 Transcription FactorIL-6R/STAT3/JAK2 pathwaymiR-451aMultiple myeloma (MM)ProliferationSTAiR18

Identifiers

PMID41204251
PMCPMC12595829

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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.