Excess administration of miR-340-5p ameliorates spinal cord injury-induced neuroinflammation and apoptosis by modulating the P38-MAPK signaling pathway

Qian, Zhiguo; Chang, Jie; Jiang, Fan; Ge, Dawei; Yang, Lei; Li, You; Chen, Hongtao

doi:10.1016/j.bbi.2020.01.025

Cited by 46 publications

(22 citation statements)

References 49 publications

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“…Immunohistochemical staining was conducted according to our previous study (Qian et al, 2020). Tissue samples were fixed, embedded, and cut into 5-µm sections.…”

Section: Immunohistochemical Stainingmentioning

confidence: 99%

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Zhang

Chen

Liu

et al. 2020

Front. Cell Dev. Biol.

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Accumulating evidence has indicated that abnormal microRNAs (miRNAs) serve critical roles in carcinogenesis and development of osteosarcoma (OS). The purpose of the present study was to elucidate the relationship between miR-766-3p and development of osteosarcoma and explore the potential mechanism. In this study, we found that miR-766-3p was the most downregulated miRNA by analyzing GSE65071 from the GEO database. miR-766-3p was lowly expressed in OS tissue samples and cells, and high miR-766-3p expression repressed the malignant level of OS, including cell proliferation, EMT, migration, and invasion in vitro and in vivo. B-Cell Lymphoma 9-Like Protein (BCL9L) was negatively associated with miR-766-3p expression in OS cells and tissue samples and was validated as the downstream target by luciferase reporter assay and western blotting. Rescue experiment indicated that BCL9L could restore the influence of miR-766-3p on OS cells. In addition, the β-Catenin/TCF-4 signal pathway was demonstrated to be related to the miR-766-3p/BCL9L axis. In summary, miR-766-3p, a negative regulator of BCL9L, plays the role of tumor metastasis suppressor via the β-catenin signaling pathway in the progression of OS.

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“…Immunohistochemical staining was conducted according to our previous study (Qian et al, 2020). Tissue samples were fixed, embedded, and cut into 5-µm sections.…”

Section: Immunohistochemical Stainingmentioning

confidence: 99%

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Zhang

Chen

Liu

et al. 2020

Front. Cell Dev. Biol.

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“…As previously demonstrated, the PI3K-Akt pathway, involved in the repair of SCI, plays an important role in the proliferation, development, differentiation, axon regeneration, myelination, apoptosis, and synaptic plasticity (53)(54)(55). The JAK-STAT, MAPK, and NODlike receptor signaling pathways are usually involved in inflammatory reactions (56)(57)(58). The functions of NTP (neuroprotection and anti-inflammation), and NM (resisting inflammation), in the treatment of SCI have been shown again through pathway analysis.…”

Section: Discussionmentioning

confidence: 99%

Cytokine expressions of spinal cord injury treated by neurotropin and nafamostat mesylate

Sun

Duan

et al. 2021

Ann Transl Med

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Background: Spinal cord injury (SCI) leads to severe physical disability and sensory dysfunction. Neurotropin (NTP) has been used clinically to alleviate neuropathic pain, while nafamostat mesylate (NM) used clinical on pancreatitis patients through inhibiting synthetic serine protease. Our previous studies showed that NTP and NM were able to repair SCI. However, the underlying mechanism has not been fully explored after treatment with these 2 different drugs. Methods:The drugs NTP and NM were administered on a contusion SCI Wistar rat model. Cytokine array analysis was performed to describe the changes of 67 proteins after acute SCI. Hierarchical clustering and volcano plot analysis were conducted to clarify protein change profiles. The differently expressed proteins related to biological processes were analyzed by functional protein association networks, Gene Ontology and pathway analysis. Flow cytometric analysis was detected to reflect the activation of immune system after drug intervention, while withdrawal threshold and BBB score were detected to evaluated the mechanical allodynia and functional recovery after SCI.Results: HGF, β-NGF, and activin were the 3 most upregulated proteins, while the receptor for RAGE, IL-1α, and TNF-α were the 3 most downregulated proteins after NTP treatment. Adiponectin, decorin and CTACK were the 3 most upregulated proteins, while RAGE, IL-1α, and IL-1β were the 3 most downregulated proteins in the NM group. Number of lymphocytes was decreased while BBB score was increased both in NTP and NM group. But only NTP could improve mechanical pain threshold after SCI. Conclusions:The PI3K-Akt, Jak-STAT signaling pathway and apoptosis might participate in SCI restoration by NTP, while the MAPK and NOD-like receptor signaling pathway may participated in repairing SCI with NM. We concluded that NTP regulated the microenvironment via a neuroprotective effect and inhibition of inflammation to repair SCI, while NM healed SCI through an anti-inflammatory effect. Both NTP and NM could down-regulate the activation of immune system and improve the functional recovery while only NTP could improve the pathological neuralgia after SCI. Elucidating the molecular mechanisms of these 2 clinical drugs indicates that they their expected to be effective clinical treatment for SCI.

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“…Alisol A treatment increased p-p38 level in MDA-MB-231 cells, which plays critical roles in mediating cellular response to stressors, and is involved in the p38-MAPK signaling pathway, thereby linking apoptosis with ROS production (26). Previous studies have shown that p38 is involved in the p38-MAPK signaling pathway and its activation is associated with cell apoptosis in different tissues (27)(28)(29)(30)(31). In the present study, the expression of the members of this signaling pathway was assessed.…”

Section: Discussionmentioning

confidence: 99%

Alisol A is potentially therapeutic in human breast cancer cells

Shi

Wang

et al. 2020

Oncol Rep

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Recent developments in breast cancer therapy have significantly improved patient survival rate; however, recurrence remains a major problem. Systemic treatment of breast cancer with available therapies is not curative. Natural products can be potentially used for treating cancer. Recently, a wide range of pharmacological activities has been reported for Alismatis Rhizoma, a popular traditional Chinese medicine. However, the mechanisms via which its compounds act on breast cancer remain unclear. The present study aimed to investigate the potential of natural therapeutic agents from Alismatis Rhizoma for treating breast cancer. Human breast cancer MDA-MB-231 cells were treated with four main protostane triterpenes from Alismatis Rhizoma, including alisol A, alisol A 24-acetate, alisol B and alisol B 23-acetate. Among these, alisol A significantly inhibited cell viability. Alisol A induced cell apoptosis, G 1 phase cell cycle arrest, autophagy, and intracellular reactive oxygen species (ROS) generation in MDA-MB-231 cells. The number of APE1-/γH2AX-/LC3-II positive cells was also significantly higher compared with that of negative control cells. All these results were dose-dependent. Cleaved caspase-3, cleaved caspase 9, Bcl-2, and p-p38 expression indicated cell apoptosis after alisol A treatment. The changes in cyclin A and cyclin D1 expression was associated with cell cycle arrest upon alisol A treatment. Furthermore, LC3-II expression upon alisol A treatment was indicative of autophagy. Alisol A treatment can induce autophagy-dependent apoptosis in human breast cancer cells via induction of ROS and DNA damage. Thus, Alisol A might serve as a new therapeutic agent against breast cancer.

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Excess administration of miR-340-5p ameliorates spinal cord injury-induced neuroinflammation and apoptosis by modulating the P38-MAPK signaling pathway

Cited by 46 publications

References 49 publications

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Cytokine expressions of spinal cord injury treated by neurotropin and nafamostat mesylate

Alisol A is potentially therapeutic in human breast cancer cells

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