MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

Hu, Yuwen; Liu, Qian; Zhang, Min; Yan, Yousheng; Yu, Hongmei; Ge, Li

doi:10.31083/j.jin.2019.01.12

Cited by 26 publications

(8 citation statements)

References 31 publications

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“…Luciferase reporter assays were performed as previously reported. 28 When the cell confluence was at 70-80%, 1 μg luciferase reporter plasmid and miR-608/miR-NC were cotransfected into U-138MG or U-251MG cells. The protein was extracted 24 hours after transfection.…”

Section: Dual-luciferase Reporter Assaymentioning

confidence: 99%

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

Wang

Hou

et al. 2020

CMAR

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Background: Glioma is one the most common and aggressive primary tumors of adult central nervous system worldwide, which tends to develop dysplasia and metastasis. Recently, toosendanin (TSN) has shown pharmacological effects in several cancers. However, little is known about the underlying mechanism of the effect of TSN on glioma and its relationship between miRNA in glioma. Methods: Cell proliferation, cell cycle, cell apoptosis and cell migration were analyzed by CCK-8 cell viability, flow cytometry, wound scratch healing, transwell and Western blotting assays, respectively, in vitro. The regulation relationships between TSN and miR-608 or between miR-608 and Notch1 (Notch2) were examined using qRT-PCR, dual-luciferase and Western blotting assays. The functional effects of TSN through regulating miR-608 and Notch1 (Notch2) were further examined using a xenograft tumor mouse model in vivo. Results: After TSN concentration was increased from 50 nM, 100 nM to 150 nM, cell proliferation and cell cycle were gradually reduced, and the cell apoptosis rate was increased in U-138MG or U-251MG cells. Wound-healing and transwell assays results showed that cell migration was significantly inhibited in TSN treatment cells (TSN treatment, 50 nM) compared to control cells. Mechanistic studies revealed that TSN up-regulated the expression of microRNA-608 (miR-608), while down-regulated the expression of miR-608's target, Notch1 and Notch2. Over-expression of Notch1 and Notch2 partly attenuated TSN-induced tumor suppressive function. Moreover, in vivo experiments revealed that TSN treatment led to a significant inhibition of tumor growth, suggesting that it might be a promising drug for the treatment of glioma. Conclusion: In the present study, a novel established functional manner of TSN/miR-608/ Notch1 (Notch2) axis was systematically indicated, which might provide prospective intervention ways for glioma therapy.

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Section: Dual-luciferase Reporter Assaymentioning

confidence: 99%

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

Wang

Hou

et al. 2020

CMAR

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“…Peripheral nerve injury often leads to refractory neuropathic pain [2,29]. Studies using animal model have demonstrated that neuropathic pain induced by peripheral nerve injury is often accompanied by apoptosis of spinal DRG neurons [30,31].…”

Section: Discussionmentioning

confidence: 99%

“…Neuropathic pain refers to the douleur anormale (abnormal pain), caused by damage and dysfunction of the central or peripheral nervous system [1,2]. Neuropathic pain is one type of chronic pain, whose main clinical manifestations include hyperalgesia, paresthesia, ambulatory pain and allodynia [3,4].…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine alleviated neuropathic pain in dorsal root ganglion neurons by inhibition of anaerobic glycolysis activity and enhancement of ROS tolerance

et al. 2020

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Neuropathic pain is a kind of chronic pain that is triggered or caused primarily by damage to the nervous system and neurological dysfunction. It’s known that dexmedetomidine is a new type of highly selective alpha2-adrenoceptor agonist with sedation, anti-anxiety, analgesic and other effects. However, the function and mechanism of dexmedetomidine on neuropathic pain are not clear. Rat DRG neurons were isolated and identified using immunofluorescence assay. Following treatment with H2O2, dexmedetomidine or ROS inhibitor (NAC), the apoptosis and ROS levels were examined by flow cytometery; apoptosis- and anaerobic glycolysis-related proteins were determined by Western blot assay; glucose consumption, pyruvic acid, lactic acid and ATP/ADP ratios were also measured. The results revealed that dexmedetomidine inhibited H2O2-induced apoptosis and reactive oxygen species (ROS) in rat DRG neurons and in addition, dexmedetomidine down-regulated the expression levels of anaerobic glycolysis-related proteins, significantly reduced glucose, pyruvic acid and lactic acid levels. It also increased the ATP/ADP ratio in H2O2-treated rat dorsal root ganglion (DRG) neurons. Moreover, we also demonstrated that ROS inhibitor (NAC) also inhibited H2O2-induced apoptosis and anaerobic glycolysis in rat DRG neurons. In conclusion, dexmedetomidine suppressed H2O2-induced apoptosis and anaerobic glycolysis activity by inhibiting ROS, in rat DRG neurons. Therefore, dexmedetomidine might play a pivotal role in neuropathic pain by the inhibition of ROS.

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“…MicroRNAs (miRNAs) belonging to a class of small non-coding RNA containing 18–25 nucleotides, which completely or partially bind the sequence of target genes, inhibit protein translation by post-transcription regulation [ 15 , 16 ]. Multiple target genes can be regulated by one single miRNA, while different miRNAs are able to affect the same gene to control protein suppression.…”

Section: Introductionmentioning

confidence: 99%

LncRNA AFAP-AS1 promotes anaplastic thyroid cancer progression by sponging miR-155-5p through ETS1/ERK pathway

et al. 2021

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Anaplastic thyroid cancer (ATC) is the most common malignant endocrine tumors which resist to majority treatment. Thus, there is impelling need to figure out the mechanism of progress of ATC. In this study, we explored the function and mechanism of lncRNA actin filamentin-1 antisense RNA (AFAP-AS1) which provided a new biomarker for ATC. Viabilities and apoptosis were tested by CCK-8, colony formation and flow cytometry. The interactions between miR-155-5p and AFAP-AS1 or ETS1 was detected by luciferase reporter assays. ETS proto-oncogene1/mitogen-activated protein kinase1 (ETS1/ERK) pathway was assessed by Western blot. Xenograft models were built to confirm the function of AFAP-AS1 in vivo. Firstly, we showed that relative RNA expression of AFAP-AS1 in ATC cells was higher than in immortalized thyroid cells. Next, AFAP-AS1 was verified as an oncogene in ATC since knock-down of AFAP-AS1 inhibited cell proliferation and accelerated apoptosis. In addition, miR-155-5p was negatively regulated by AFAP-AS1. Moreover, AFAP-AS1 regulated ETS1/ERK pathway by sponging miR-155-5p. Finally, we confirmed knock-down of AFAP-AS1 significantly suppressed tumor proliferation in vivo. Our research proved that AFAP-AS1 could facilitate progression of thyroid cancer sponging miR-155-5p through ETS1/ERK pathway.

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MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

Abstract: J o u r n a l o f I n t e g r a t i v e N e u r o s c i e n c e

Cited by 26 publications

References 31 publications

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

<p>Toosendanin Suppresses Glioma Progression Property and Induces Apoptosis by Regulating miR-608/Notch Axis</p>

Dexmedetomidine alleviated neuropathic pain in dorsal root ganglion neurons by inhibition of anaerobic glycolysis activity and enhancement of ROS tolerance

LncRNA AFAP-AS1 promotes anaplastic thyroid cancer progression by sponging miR-155-5p through ETS1/ERK pathway

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