MicroRNA-31 Negatively Regulates Interleukin-34 Expression In Vitro

Li, Miaomiao; Dong, Yan; Chen, Zhangming; Li, Meng; Liu, Xingyun; Zhang, Xinhui; Wang, Huimin; Mao, Weijia; Zhang, Jie; Jiang, Zhe; Huang, Ting; Hu, Jie; Luo, Pei; Korner, Heinrich; Shi, Ying; Li, Jun

doi:10.1080/08820139.2019.1578230

Cited by 7 publications

(2 citation statements)

References 37 publications

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“…Interestingly, miR-31 targets IL34 to reduce its expression. 28 Thus, it would be interesting to study miR-31 expression in our cells to evaluate the possible relation with IL34 expression and with the deletion of CDKN2A. miR-31 is usually dysregulated in cancer; however, it could act either as a tumor suppressor or as an oncogene.…”

Section: Open Accessmentioning

confidence: 99%

Involvement of the M-CSF/IL-34/CSF-1R pathway in malignant pleural mesothelioma

Blondy

D'Almeida

Briolay

et al. 2020

J Immunother Cancer

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BackgroundMalignant pleural mesothelioma (MPM) is a rare and aggressive cancer related to asbestos exposure. The tumor microenvironment content, particularly the presence of macrophages, was described as crucial for the development of the disease. This work aimed at studying the involvement of the M-CSF (CSF-1)/IL-34/CSF-1R pathway in the formation of macrophages in MPM, using samples from patients.MethodsPleural effusions (PEs), frozen tumors, primary MPM cells and MPM cell lines used in this study belong to biocollections associated with clinical databases. Cytokine expressions were studied using real-time PCR and ELISA. The Cancer Genome Atlas database was used to confirm our results on an independent cohort. An original three-dimensional (3D) coculture model including MPM cells, monocytes from healthy donors and a tumor antigen-specific cytotoxic CD8 T cell clone was used.ResultsWe observed that high interleukin (IL)-34 levels in PE were significantly associated with a shorter survival of patients. In tumors, expression of CSF1 was correlated with ‘M2-like macrophages’ markers, whereas this was not the case with IL34 expression, suggesting two distinct modes of action of these cytokines. Expression of IL34 was higher in MPM cells compared with primary mesothelial cells. Particularly, high expression of IL34 was observed in MPM cells with an alteration of CDKN2A. Finally, using 3D coculture model, we demonstrated the direct involvement of MPM cells in the formation of immunosuppressive macrophages, through activation of the colony stimulating factor-1 receptor (CSF1-R) pathway, causing the inhibition of cytotoxicity of tumor antigen-specific CD8+ T cells.ConclusionsThe M-CSF/IL-34/CSF-1R pathway seems strongly implicated in MPM and could constitute a therapeutic target to act on immunosuppression and to support immunotherapeutic strategies.

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Section: Open Accessmentioning

confidence: 99%

Involvement of the M-CSF/IL-34/CSF-1R pathway in malignant pleural mesothelioma

Blondy

D'Almeida

Briolay

et al. 2020

J Immunother Cancer

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“…Studies showed that microglia are involved in the formation of protective scarring during SCI repair, which protects neurons after SCI. 45,46 On the other hand, the high expression of miR-31 will negatively regulate IL-34 expression, 47 which may inhibit the proliferation of microglia and reduce the neuroprotection of microglia after SCI. In addition, decreased vitamin D is detrimental to the repair of SCI, 48,49 which was confirmed by Zhang et al, who showed that vitamin D could upregulate IL-34 in SH-SY5Y neural cells.…”

Section: Discussionmentioning

confidence: 99%

miR-31 promotes neural stem cell proliferation and restores motor function after spinal cord injury

Gao

Tian

et al. 2021

Exp Biol Med (Maywood)

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This study aims to examine whether miR-31 promotes endogenous NSC proliferation and be used for spinal cord injury management. In the present study, the morpholino knockdown of miR-31 induced abnormal neuronal apoptosis in zebrafish, resulting in impaired development of the tail. miR-31 agomir transfection in NSCs increased Nestin expression and decreased ChAT and GFAP expression levels. miR-31 induced the proliferation of mouse NSCs by upregulating the Notch signaling pathway, and more NSCs entered G1; Notch was inhibited by miR-31 inactivation. Injection of a miR-31 agomir into mouse models of spinal cord injury could effectively restore motor functions after spinal cord injury, which was achieved by promoting the proliferation of endogenous NSCs. After the injection of a miR-31 agomir in spinal cord injury mice, the expression of Nestin and GFAP increased, while GFAP expression decreased. In conclusion, the zebrafish experiments prove that a lack of miR-31 will block nervous system development. In spinal cord injury mouse models, miR-31 overexpression might promote spinal cord injury repair.

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