Evidence map›Paper›PMID 35444864›Full record

ArticlePeerJ2022

miR-34a-5p inhibits the malignant progression of KSHV-infected SH-SY5Y cells by targeting c-fos.

Shuyuan Wu, Zhaofu Wu, Huiling Xu, Jinli Zhang, Wenyi Gu, Xiaohua Tan, Zemin Pan, Dongdong Cao, Dongmei Li, Lei Yang and 2 more

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.3field-weighted citation impact, top 6% of its field
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

10 citing papers in PubMed, 29 citations in OpenAlex.

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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

12 authors at 4 institutions in 2 countries.

Shuyuan Wu *Key Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Zhaofu Wu *Key Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Huiling XuKey Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Jinli ZhangKey Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Wenyi GuAustralian Institute for Bioengineering and Nanotechnology (AIBN), University of Queensland (UQ), St Lucia, Brisbane, Australia.
Xiaohua TanSchool of Medicine, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Zemin PanKey Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Dongdong CaoKey Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Dongmei LiKey Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Lei YangSchool of Medicine, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Dongmei LiKey Laboratory of Xinjiang Endemic and Ethnic Diseases/NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Yuanming PanDepartment of Cellular and Molecular Biology, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, Beijing, China.
Shihezi University · CNHangzhou Normal University · CNCapital Medical University · CNUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: We aimed to investigate the effects of miR-34a-5p on c-fos regulation mediating the malignant behaviors of SH-SY5Y cells infected with Kaposi's sarcoma-associated herpesvirus (KSHV). Methods: The KSHV-infected (SK-RG) and uninfected SH-SY5Y parent cells were compared for differentially expressed miRNAs using transcriptome sequencing. Then miR-34a-5p was upregulated in SK-RG cells by the miRNA mimics transfection. Cell proliferation ability was determined by MTT and plate clone assays. The cell cycle was assessed by flow cytometry analysis, and CDK4, CDK6, cyclin D1 levels were determined by Western blot analysis. The migration behavior was detected by wound healing and transwell assays. The protein levels of MMP2 and MMP9 were measured by Western blot analysis. The regulation of c-fos by miR-34a-5p was detected by the dual-luciferase reporter gene assay. Rescue assays were carried out by upregulating c-fos in miR-34a-5p-overexpressing SK-RG cells. KSHV DNA copy numbers and relative virus gene expressions were detected. Xenograft tumor experiments and immunohistochemistry assays were further used to detect the effects of miR-34a-5p. Results: miR-34a-5p was lower in SK-RG cells. Restoration of miR-34a-5p decreased cell proliferation and migration, leading to a G1 cell cycle arrest and down-regulation of CDK4/6, cyclin D1, MMP2, MMP9. KSHV copy number and expression of virus gene including latency-associated nuclear antigen (LANA), replication and transcription activator (RTA), open reading frame (K8.1), and KSHV G protein-coupled receptor (v-GPCR) were also reduced. Furthermore, c-fos is the target of miR-34a-5p, while enhanced c-fos weakened cellular behaviors of miR-34a-5p-overexpressing cells. Xenograft experiments and immunohistochemistry assays showed that miR-34a-5p inhibited tumor growth and virus gene expression. Conclusion: Upregulated miR-34a-5p in KSHV-infected SH-SY5Y cells suppressed cell proliferation and migration through down-regulating c-fos. miR-34a-5p was a candidate molecular drug for KSHV-infected neuronal cells.

Indexed as

Herpesvirus 8, HumanMicroRNAsNeuroblastomaAnimalsCyclin D1HumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9Cyclin D1Matrix Metalloproteinase 2Matrix Metalloproteinase 9MicroRNAsMIRN34 microRNA, humanc-fosKaposi’s sarcoma–associated herpesvirusMigrationmiR-34a-5pProliferation

Identifiers

PMID35444864
PMCPMC9014853
OpenAlexW4224118722

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.