MicroRNA-93-5p may participate in the formation of morphine tolerance in bone cancer pain mouse model by targeting Smad5

Xiao, Wenfeng; Li, Yusheng; Lou, Wei; Cai, Ting; Zhang, Shun; Hu, Xiaoying; Zhang, Xingwang; Luo, Wei

doi:10.18632/oncotarget.10524

Cited by 17 publications

(17 citation statements)

References 41 publications

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“…In the present study, we demonstrated that the expression of miR-93 was significantly increased in NPC cell lines and tumor tissues. The evidence indicates that miR-93 was upregulated in NPC, which is consistent with the results obtained from bone cancer ( 15 ), myocardial ischemia/reperfusion (I/R) injury ( 14 ) and polycystic ovarian syndrome ( 22 ). The enhanced proliferation of NPC cell lines indicated that miR-93 was an oncogene in NPC.…”

Section: Discussionsupporting

confidence: 88%

“…These findings indicated that the abnormally expressed miRNAs may contribute to the progression and development of NPC. miR-93, derived from a paralogue (miR-106b-25), is dysregulated in several cancer types, such as epithelial ovarian carcinoma ( 13 ), ischemic heart disease ( 14 ) and bone cancer pain mouse model ( 15 ). The evidence indicates that miR-93 plays a key role in cancer progression.…”

Section: Introductionmentioning

confidence: 99%

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miR-93 enhances cell proliferation by directly targeting CDKN1A in nasopharyngeal carcinoma

Zhang

2017

Oncol Lett

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Nasopharyngeal carcinoma (NPC) is an epithelial malignancy of the head and neck with the highest incidence rate in southern China. The aim of the present study was to understand the molecular mechanisms that underlie the progression of NPC. The relative expression of miR-93 and CDKN1A was detected by the reverse-transcription quantitative PCR. Western blot analysis was applied to detect the protein levels of genes. Luciferase activity report was applied to verify the target of miRNA. Cell growth was assayed by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. miR-93 was upregulated in NPC tissues and cell lines compared with normal samples. Re-expression of miR-93 promoted cell growth in vitro as determined by the MTT assay. CDKN1A was identified by luciferase reporter as a direct target of miR-93. Its expression was downregulated by miR-93. Furthermore, the results showed that the expression of miR-93 was inversely correlated with the expression of CDKN1A protein. miR-93 enhanced cell proliferation in NPC by directly targeting CDKN1A. It is suggested that miR-93/CDKN1A axis may present a new target for the treatment of NPC.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

miR-93 enhances cell proliferation by directly targeting CDKN1A in nasopharyngeal carcinoma

Zhang

2017

Oncol Lett

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“…Similarly, high expression of miR-195 suppresses tumor growth in prostate carcinoma in vivo (42). SMAD5 could serve as a target of miRNA to inhibit the angiogenesis, thereby contributing to tumor growth and metastases (43).…”

Section: Discussionmentioning

confidence: 99%

Silencing of Long Non-coding RNA SMAD5-AS1 Reverses Epithelial Mesenchymal Transition in Nasopharyngeal Carcinoma via microRNA-195-Dependent Inhibition of SMAD5

Zhao

Shang

et al. 2019

Front. Oncol.

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Long non-coding RNAs (lncRNAs) have gained widespread attention in recent years as a key regulator of diverse biological processes, but the knowledge of the mechanisms by which they act is still very limited. Differentially expressed lncRNA SMAD5 antisense RNA 1 (SMAD5-AS1) in nasopharyngeal carcinoma (NPC) and normal samples shown by in silico analyses were selected as the main subject, and then was suggested to bind to SMAD5-AS1 and SMAD5. Therefore, the purpose of the present study was to investigate the effects of SMAD5-AS1/miR-195/SMAD5 on epithelial-mesenchymal transition (EMT) in NPC cells. High expression of SMAD5-AS1 and SMAD5 but low miR-195 expression was determined in NPC tissues and NPC cell lines by RT-qPCR and western blot analysis. SMAD5-AS1 could upregulate SMAD5 expression by competitively binding to miR-195 in NPC cells. Loss-and gain-of-function investigations were subsequently conducted in NPC cells (CNE-2 and CNE-1) to explore the role of SMAD5-AS, miR-195 and SMAD5 in NPC progression by assessing cellular biological functions and tumorigenic ability in vivo as well as determining the expression of EMT markers. Downregulation of SMAD5-AS1 or SMAD5 or overexpression of miR-195 led to inhibited NPC cell proliferation, invasion and migration and reversed EMT, enhanced apoptosis in vitro as well as restrained tumor growth in vivo. In conclusion, our findings indicate that silencing of lncRNA SMAD5-AS1 induces the downregulation of SMAD5 by miR-195, eventually repressing EMT in NPC. Hence, SMAD5-AS1 may represent a potential therapeutic target for NPC intervention.

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“…Moreover, anti-miR-93 alleviated morphine tolerance. Overall, Up-regulation of miR-93 may contribute to the progression of morphine tolerance by targeting Smad5 in mouse bone cancer pain (Xiao et al, 2016 ). Morphine tolerance was remarkably suppressed in pLV-THM-miR-338 rats with lower expression of CXC chemokine receptor-4 (CXCR4).…”

Section: Relevance Of Mirna-based Mechanisms In Morphine Tolerancementioning

confidence: 99%

The Regulatory Mechanisms and Therapeutic Potential of MicroRNAs: From Chronic Pain to Morphine Tolerance

Dai

et al. 2018

Front. Mol. Neurosci.

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Chronic pain, including cancer-related pain, is a pain condition often caused by inflammation or dysfunctional nerves. Chronic pain treatment poses a significant health care challenge, where opioids especially morphine are widely used and patients often develop tolerance over time with aggravated pain. microRNA (miRNA) is known to play important roles in regulating gene expressions in the nervous system to affect neuronal network plasticity related to algogenesis and the developing of morphine tolerance. In this article, we reviewed studies conducted in rodent animal models investigating the mechanisms of miRNAs regulation in chronic pain with different phenotypes and morphine tolerance. In addition, the potential of targeting miRNAs for chronic pain and morphine tolerance treatment is also reviewed. Finally, we point out the directions of the future research in chronic pain and morphine tolerance.

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MicroRNA-93-5p may participate in the formation of morphine tolerance in bone cancer pain mouse model by targeting Smad5

Cited by 17 publications

References 41 publications

miR-93 enhances cell proliferation by directly targeting CDKN1A in nasopharyngeal carcinoma

miR-93 enhances cell proliferation by directly targeting CDKN1A in nasopharyngeal carcinoma

Silencing of Long Non-coding RNA SMAD5-AS1 Reverses Epithelial Mesenchymal Transition in Nasopharyngeal Carcinoma via microRNA-195-Dependent Inhibition of SMAD5

The Regulatory Mechanisms and Therapeutic Potential of MicroRNAs: From Chronic Pain to Morphine Tolerance

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