Effects of <i>miR-338</i> on morphine tolerance by targeting CXCR4 in a rat model of bone cancer pain

Mei, Hongxia; Zhou, Min-Hong; Zhang, Xingwang; Huang, Xixi; Wang, Yongle; Wang, Peifang; Gao, Zhan

doi:10.1042/bsr20160517

Cited by 19 publications

(16 citation statements)

References 33 publications

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“…The negative plates were developed with a developing agent (CAS item 7757‐83‐7; Hefei Jiankun Chemical Co, Ltd, Hefei, China). The degree of bone destruction induced by tumor was evaluated . Experiments of each group were repeated in triplicate.…”

Section: Methodsmentioning

confidence: 99%

Retracted: Analgesic effects of microRNA‐129‐5p against bone cancer pain through the EphB1/EphrinB2 signaling pathway in mice

Zhao

et al. 2017

J of Cellular Biochemistry

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The study aims to investigate the analgesic effects of microRNA-129-5p (miR-129-5p) on bone cancer pain (BCP) by targeting Eph receptor B1 (EphB1) through the EphB1/EphrinB2 signaling pathway. BCP mice models were established, and C3H/HeJ female mice were classified into the normal, blank, negative control (NC), miR-129-5p mimics, miR-129-5p inhibitors, EphB1 knockout (KO), and miR-129-5p inhibitors + EphB1 KO groups. Quantitative reverse transcription polymerase chain reaction and Western blot analysis were used to evaluate the miR-129-5p expression, and messenger RNA (mRNA) and protein expressions of EphB1, p-EphB1, EphrinB2, and p-EphrinB2. EphB1 and EphrinB2 were highly activated in the tibias of BCP mice 7 days after the operation. EphB1 is a target gene of miR-129-5p. The mechanical withdrawal threshold increased in the miR-129-5p mimics, EphB1 KO and miR-129-5p inhibitors + EphB1 KO groups, but decreased in the miR-129-5p inhibitors group. Compared with the blank and the NC groups, the expression of miR-129-5p was significantly increased in the miR-129-5p mimics group, and the mRNA and protein expressions of EphrinB2, p-EphrinB2, EphB1, and p-EphB1 were significantly decreased, while in the miR-129-5p inhibitors group, the results were opposite (all P< 0.05); the mRNA and protein expressions of EphrinB2, p-EphrinB2, EphB1, and p-EphB1 were significantly decreased in the EphB1 KO group (all P < 0.05); the expression of miR-129-5p was significantly decreased in the miR-129-5p inhibitors + EphB1 KO group ( P < 0.05), while the mRNA and protein expressions of EphrinB2 and p-EphrinB2 were not significantly different ( P > 0.05). The results indicated that upregulated miR-129-5p alleviate BCP via downregulation of the EphB1/EphrinB2 signaling pathway.

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Section: Methodsmentioning

confidence: 99%

Retracted: Analgesic effects of microRNA‐129‐5p against bone cancer pain through the EphB1/EphrinB2 signaling pathway in mice

Zhao

et al. 2017

J of Cellular Biochemistry

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“…For example, miR-365 could reverse morphine tolerance via inhibiting b-arrestin 2 expression in the spinal cord; 8 miR-375 could signicantly hinder morphine tolerance via inhibiting JAK2/STAT3 pathway; 28 miR-93 may be involved in the tolerance by targeting Smad5; 29 miR-338 could suppress the tolerance by targeting CXCR4. 30 In our study, we found that miR-26b was decreased during the morphine tolerance, and miR-26b-mimic could attenuate the tolerance signicantly.…”

Section: Discussionmentioning

confidence: 52%

Retracted Article: Upregulation of miR-26b alleviates morphine tolerance by inhibiting BDNF via Wnt/β-catenin pathway in rats

Liu

Geng

et al. 2019

RSC Adv.

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“…Morphine tolerance was remarkably suppressed in pLV-THM-miR-338 rats with lower expression of CXC chemokine receptor-4 (CXCR4). Although the specific mechanisms of miR-338 targeting of CXCR4 was unknown, miR-338 significantly influenced the inhibition of morphine tolerance (Mei et al, 2017 ).…”

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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Effects of miR-338 on morphine tolerance by targeting CXCR4 in a rat model of bone cancer pain

Cited by 19 publications

References 33 publications

Retracted: Analgesic effects of microRNA‐129‐5p against bone cancer pain through the EphB1/EphrinB2 signaling pathway in mice

Retracted: Analgesic effects of microRNA‐129‐5p against bone cancer pain through the EphB1/EphrinB2 signaling pathway in mice

Retracted Article: Upregulation of miR-26b alleviates morphine tolerance by inhibiting BDNF via Wnt/β-catenin pathway in rats

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

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