miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

Li, Bo; Wang, Zhijie; Yu, Mei; Wang, Xu; Wang, Xin; Chen, Chuanjie; Zhang, Zheng; Zhang, Meiling; Sun, Chao; Zhao, Chenxi; Li, Qiang; Wang, Wei; Wang, Tianyi; Zhang, Liang; Ning, Guangzhi; Feng, Shiqing

doi:10.1002/jcp.29338

Cited by 23 publications

(21 citation statements)

References 60 publications

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“…Thus, there could be other miRNAs downstream melatonin. After literature research, we chose miR-21, miR-133a, miR-148a-3p, miR-25-5p, and miR-155, which have been reported to regulate tumor progression in other cancers and MiRNAs, a cluster of noncoding RNAs, could regulate cell biological behaviors in tumors via targeting the 3'UTR of target genes (61). The role of miRNAs has been studied in multi tumors like breast and colon cancers (62,63).…”

Section: Discussionmentioning

confidence: 99%

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Melatonin Inhibits the Progression of Oral Squamous Cell Carcinoma via Inducing miR-25-5p Expression by Directly Targeting NEDD9

Wang¹,

Tao

Mao

et al. 2020

Front. Oncol.

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Melatonin exerts anti-cancer roles in various types of cancers. However, to the best of our knowledge, its role in oral squamous cell carcinoma (OSCC) is unknown. The present study aimed to investigate the role of melatonin and its underlying mechanism in OSCC. MTT, colony formation, wound healing, and transwell invasion assays proved that melatonin played anti-tumor effects in OSCC cells by inhibiting cell viability, proliferation, migration, and invasion in a concentration-dependent manner. The RT-qPCR analysis showed that miR-25-5p was significantly upregulated after melatonin treatment. Further, miR-25-5p might be involved in melatonin-induced inhibitory effects on the biological behavior of OSCC. The expression of miR-25-5p was decreased in tumor tissues and OSCC cells detected by RT-qPCR. MTT assay, colony formation assay, and TUNEL staining indicated miR-25-5p overexpression inhibited OSCC cell viability, proliferation, and induced OSCC cell apoptosis. Furthermore, wound healing, transwell invasion assay, and animal experiments suggested that miR-25-5p might exert suppressive effects on the migration, invasion, and tumor formation of OSCC cells, while miR-25-5p knockdown exhibited the opposite effects in OSCC cells. Bioinformatics analysis, western blot analysis, and luciferase reporter assay suggested that neural precursor cell expressed developmentally downregulated protein 9 (NEDD9) was proved to be a putative target for miR-25-5p. The role of NEDD9 in inhibiting OSCC cell proliferation, invasion, and migration was verified with NEDD9 siRNA transfection. Thus, melatonin exerted anti-proliferative, anti-invasive, and anti-migrative effects on OSCC via miR-25-5p/NEDD9 pathway. Melatonin could be applied as a potential novel drug on treating OSCC.

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Section: Discussionmentioning

confidence: 99%

“…MiRNAs, a cluster of noncoding RNAs, could regulate cell biological behaviors in tumors via targeting the 3’UTR of target genes ( 61 ). The role of miRNAs has been studied in multi tumors like breast and colon cancers ( 62 , 63 ).…”

Section: Discussionmentioning

confidence: 99%

Melatonin Inhibits the Progression of Oral Squamous Cell Carcinoma via Inducing miR-25-5p Expression by Directly Targeting NEDD9

Wang¹,

Tao

Mao

et al. 2020

Front. Oncol.

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“…Furthermore, miR-22-3p mimic was observed to raise the levels of phosphor-STAT3 (p-STAT3) and phosphor-growth-associated protein 43 (p-GAP-43). Also in vivo, miR-22-3p could improve EGFR signaling and restore spinal cord sensory conductive function through CBL/p-EGFR/p-STAT3/GAP43/p-GAP43 axis regulation [ 126 ].…”

Section: Mirnas For Neuronal Regeneration In Scimentioning

confidence: 99%

MiRNAs as Promising Translational Strategies for Neuronal Repair and Regeneration in Spinal Cord Injury

Silvestro

Mazzon

2022

Cells

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Spinal cord injury (SCI) represents a devastating injury to the central nervous system (CNS) that is responsible for impaired mobility and sensory function in SCI patients. The hallmarks of SCI include neuroinflammation, axonal degeneration, neuronal loss, and reactive gliosis. Current strategies, including stem cell transplantation, have not led to successful clinical therapy. MiRNAs are crucial for the differentiation of neural cell types during CNS development, as well as for pathological processes after neural injury including SCI. This makes them ideal candidates for therapy in this condition. Indeed, several studies have demonstrated the involvement of miRNAs that are expressed differently in CNS injury. In this context, the purpose of the review is to provide an overview of the pre-clinical evidence evaluating the use of miRNA therapy in SCI. Specifically, we have focused our attention on miRNAs that are widely associated with neuronal and axon regeneration. “MiRNA replacement therapy” aims to transfer miRNAs to diseased cells and improve targeting efficacy in the cells, and this new therapeutic tool could provide a promising technique to promote SCI repair and reduce functional deficits.

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“…To detect the protein expression of NRF2, Histone 3 (H3), β-acting, HO-1, kelch like ECH associated protein 1 (Keap1), Bax B-Cell CLL/Lymphoma 2 (Bcl-2), Bcl2 associated X, apoptosis regulator (Bax) and cleaved caspase 3 in the myocardial tissues and cultured HL-1 cells, western blotting was conducted as previously reported (16,17).…”

Section: Western Blottingmentioning

confidence: 99%

3'-daidzein sulfonate protects myocardial cells from hypoxic-ischemic injury via the NRF2/HO-1 signaling pathway

Zeng¹,

Yu²,

Zeng³

et al. 2021

J Thorac Dis

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Background: Myocardial infarction (MI) has a high mortality and disability rate and greatly affects human health. This study sought to explore the therapeutic effect and molecular mechanism of 3'-daidzein sulfonate (DSS) on MI. Methods: A rat MI model was established and low and high doses of DSS were administered to the rats. An in vitro oxygen glucose deprivation model was used to verify the treatment role and mechanism of DSS. The establishment of the rat MI model was confirmed by electrocardiogram. The tissue changes were detected by HE, Masson's trichrome, TUNEL and TTC staining. Cell viability was detected by CCK-8. The viable and dead cells were detected by Calcein-AM/PI. Apoptotic cells, ROS and JC-1 were detected by flow cytometry apoptosis. The level of proteins was detected by western blotting. MDA, SOD and GSH were detected by ELISA. Results: The results of Hematoxylin and eosin, TUNEL, and Masson staining showed that the myocardial tissue of the MI group was repaired by DSS. The serum levels of cardiac troponin I (CTnI), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and malondialdehyde (MDA) were decreased by DSS, while the serum levels of superoxide dismutase and glutathione were promoted by DSS. The treatment of DSS activated the Nuclear Factor Erythroid 2-Related Factor 2 (NRF-2)/Heme Oxygenase 1 (HO-1) pathway and inhibited the caspase-3 apoptosis pathway. The in vitro experiment showed that DSS greatly restored cell viability and reduced cell apoptosis. DSS also greatly inhibited mitochondrial membrane potential depolarization, reactive oxygen species production, and oxidative stress. The application of the NRF-2 inhibitor, C 29 H 25 N 3 O 4 S (ML385), greatly inhibited the treatment role of DSS and the NRF-2/HO-1 pathway, and activated the caspase-3 apoptosis pathway. Conclusions: In conclusion, this study first identified the beneficial role of DSS in MI. DSS protected myocardial cells by activating the NRF-2/HO-1 pathway and inhibiting cell apoptosis. DSS could be used as a novel drug in the treatment of MI.

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miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

Cited by 23 publications

References 60 publications

Melatonin Inhibits the Progression of Oral Squamous Cell Carcinoma via Inducing miR-25-5p Expression by Directly Targeting NEDD9

Melatonin Inhibits the Progression of Oral Squamous Cell Carcinoma via Inducing miR-25-5p Expression by Directly Targeting NEDD9

MiRNAs as Promising Translational Strategies for Neuronal Repair and Regeneration in Spinal Cord Injury

3'-daidzein sulfonate protects myocardial cells from hypoxic-ischemic injury via the NRF2/HO-1 signaling pathway

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