<i>Retracted</i>: Analgesic effects of microRNA‐129‐5p against bone cancer pain through the EphB1/EphrinB2 signaling pathway in mice

Yu, Shiying; Li, Longyun; Zhao, Guoqing; Liu, Lin; Li, Xuefeng

doi:10.1002/jcb.26605

Cited by 6 publications

(3 citation statements)

References 41 publications

(87 reference statements)

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“…MiR-129 has long been studied as a biomarker for cancers such as gastric, rectal, and bladder cancer. In this signaling pathway in mice (33). Our results confirmed that miR-129 may be closely related to the analgesic effect of morphine.…”

Section: Discussionsupporting

confidence: 77%

Molecular mechanism and candidate biomarkers of morphine for analgesia and addiction effects

Wang¹,

Chen²,

Zeng³

2022

Ann Transl Med

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Background: Morphine and its substitutes are frequently used in the clinical treatment of acute severe pain and advanced cancer patients. Long-term irregular use of morphine will lead to severe dependence.However, the genes behind the analgesic and addictive effects of morphine still need to be revealed. Methods:We retrieved and downloaded RNA expression data sets related to morphine pain and addiction effects from the Gene Expression Omnibus (GEO) database to identify differentially expressed genes.Functional enrichment analysis was performed to analyze relevant pathways. Gene expression trends was used to screen key genes associated with addiction effects. miRNAs and PPIs were used to explore the functional mechanisms of genes.Results: A total of 163 up-regulated and 277 down-regulated genes were obtained in the dataset for analgesic effects. A total of 1,482 up-regulated and 1,754 down-regulated differentially expressed genes (DEGs) were obtained in the dataset for addictive effects. By taking the intersection, 8 up-regulated and 22 down-regulated mRNAs which showed high correlations with both analgesic and addictive effects were identified. Based on the DEGs, a comprehensive network combining the mRNA-miRNA network and protein-protein interaction (PPI) network was established. Among the networks, 1 up-regulated miRNA (miR-129) and 3 down-regulated miRNAs (miR-714, miR-2135, and miR-2145) were identified. Gene expression trends and Kyoto Encyclopedia of Genes and Genomes (KEGG) terms indicated that Fos may be a biomarker for morphine addiction.Conclusions: Our findings will provide a valuable foundation for future genetic mechanism studies of the analgesic and addictive effects of morphine and provide inspiration for finding analgesic substitutes and relieving the addiction of analgesic drugs.

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Section: Discussionsupporting

confidence: 77%

Molecular mechanism and candidate biomarkers of morphine for analgesia and addiction effects

Wang¹,

Chen²,

Zeng³

2022

Ann Transl Med

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“…The pathogenesis of BCP is related to a multitude of genetical and biological regulators [3,4], however, recently an increasing amount of evidence support that microRNAs (miRNAs) play an essential role as regulators in BCP development [5][6][7][8]. MiRNAs can regulate multiple pathological and physiological processes, including differentiation, morphogenesis, apoptosis, proliferation, and survival on the protein level, through binding to the 3' untranslated region of their target mRNAs [9].…”

Section: Introductionmentioning

confidence: 99%

MiR-135-5p Alleviates Bone Cancer Pain by Regulating Astrocyte-Mediated Neuroinflammation in Spinal Cord through JAK2/STAT3 Signaling Pathway

et al. 2021

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Bone cancer pain (BCP) was associated with microRNA dysregulation. In this study, we intended to clarify the potential role of miR-135-5p in a BCP mouse model, which was established by tumor cell implantation (TCI) in the medullary cavity of the mouse femur. The BCP related behaviors were tested, including the paw withdrawal mechanical threshold (PWMT) and number of spontaneous flinches (NSF). The miRNA expression profiles in astrocytes of the sham and tumor groups were compared, and miRNA microarray and quantitative real-time PCR (qRT-PCR) assays confirmed that the amount of expression of miR-135-5p was significantly decreased in astrocytes of the tumor group. Gain-and loss-of-function studies showed that miR-135-5p could inhibit astrocytes activation and inflammation cytokines (TNF-α and IL-1β) expression. The relation between miR-135-5p and JAK2 was detected by bioinformatic analysis and dual luciferase reporter gene assay. By conducting in vitro experiments, it was shown that the miR-135-5P mimics lowered the level of JAK2/STAT3 proteins and inflammatory factors in astrocytes. Moreover, in vivo analysis on BCP mice model indicated that the miR-135-5p agonist could sufficiently increase PWMT and decrease NSF. Meanwhile, reduced activation of astrocytes in the spinal cord, as well as decreased expression of JAK2/STAT3 and inflammatory mediators, were found after miR-135-5p agonist treatment. Collectively, the results showed that miR-135-5p could potentially reduce BCP in mice through inhibiting astrocyte-mediated neuroinflammation and blocking of the JAK2/STAT3 signaling pathway, indicating that the upregulation of miR-135-5P could be a therapeutic focus in BCP treatment.

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“…MiR-125b was chosen for further study, and the authors found that miR-125b was essential for functional recovery, and it guides correct regeneration of axons through the lesion site via direct downstream target Sema4D in axolotls [14]. MiR-129-5p acts as a tumor suppressor and has been widely studied in different cancer including colon cancer [15], non-small cell lung cancer [16], bone cancer [17], and breast cancer [18]. However, the role of miR-129-5p in the acute SCI still remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of MiR-129-5p on Acute Spinal Cord Injury Rats

Yang

Cai

et al. 2019

Med Sci Monit

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Departmental sources Background: Spinal cord injury (SCI) is a severe devastating condition associated with serious disability and neurologic deficits. Aberrant micro RNA (miRNA) expression has been related to a variety of central nervous system diseases including SCI. In the present study, we aimed to discover the role of miR-129-5p on SCI. Material/Methods: An acute SCI rat model was induced, following the modified Allen method. A total of 36 rats were randomly assigned into 4 groups (n=9 in every group): Sham group; Model group (SCI+saline); SCI+NC group; and SCI+miR-129-5p group (100 nm solution, every 2 days). Basso-Beattie-Bresnahan (BBB) locomotor rating score was carried out to determine functional recovery. TUNEL (terminal dUTP nick-end labeling) staining was used to evaluate cell apoptosis. Hematoxylin and eosin staining was performed to assess the pathological state of spinal cord. Furthermore, western blot assay was conducted to measure the calpain1 and calpain2 expression. Results: Our data suggested that the expression level of miR-129-5p was markedly reduced in rats after SCI. Then miR-129-5p mimic was injected into the vertebral canal. We found that the SCI+miR-129-5p group had a high score in the BBB test compared with the SCI+NC group and the Model group. The overexpression of miR-129-5p obviously reduced tissue loss, damaged cells, and the number of TUNEL positive cells. Moreover, western blot assay exhibited that overexpression of miR-129-5p decreased calpain1, calpain2, and cleaved caspase-3 expression. Conclusions: Our findings suggested that overexpression of miR-129-5p improved neurological function by promoting functional recovery, reducing tissue loss and cell apoptosis in rats in an SCI model, possibly through downregulation of calpain1 and calpain2.

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Retracted: Analgesic effects of microRNA‐129‐5p against bone cancer pain through the EphB1/EphrinB2 signaling pathway in mice

Cited by 6 publications

References 41 publications

Molecular mechanism and candidate biomarkers of morphine for analgesia and addiction effects

Molecular mechanism and candidate biomarkers of morphine for analgesia and addiction effects

MiR-135-5p Alleviates Bone Cancer Pain by Regulating Astrocyte-Mediated Neuroinflammation in Spinal Cord through JAK2/STAT3 Signaling Pathway

Protective Effects of MiR-129-5p on Acute Spinal Cord Injury Rats

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