Research Papers:

Long non-coding RNA CCAT1 modulates neuropathic pain progression through sponging miR-155

Lidong Dou, Hongqi Lin _, Kaiwei Wang, Guosong Zhu, Xuli Zou, Enqiang Chang and Yongfeng Zhu

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Oncotarget. 2017; 8:89949-89957. https://doi.org/10.18632/oncotarget.21192

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Lidong Dou1, Hongqi Lin1, Kaiwei Wang1, Guosong Zhu1, Xuli Zou1, Enqiang Chang1 and Yongfeng Zhu1

1Department of Anesthesiology, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, China

Correspondence to:

Hongqi Lin, email: [email protected]

Keywords: neuropathic pain, long non-coding RNAs, lncRNAs, CCAT1, miR-155

Received: June 04, 2017    Accepted: July 07, 2017    Published: September 23, 2017


Neuropathic pain is caused by dysfunction or primary injury of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) play important roles in the development of neuropathic pain. However, the effects of lncRNA colon cancer associated transcript-1 (CCAT1) in neuropathic pain have not been reported. The model of bilateral sciatic nerve chronic constriction injuries (bCCI) is regarded as long-lasting mechanical hypersensitivity and cold allodynia, which is the representative symptom in the human subjects suffering from the neuropathic pain. In this study, we found that CCAT1 expression was decreased in the spinal dorsal horn, dorsal root ganglion (DRG), hippocampus, and anterior cingulate cortex (ACC) of rats with bCCI. The rats of bCCI presented the cold allodynia after the 14th day of postoperation. We furtherly showed that lncRNA CCAT1 decreased miR-155 expression and enhanced Serum and glucocorticoid regulated protein kinase 3 (SGK3) expression in the NGF-differentiated PC12 cell. We found that miR-155 expression was increased in the spinal dorsal horn, DRG, hippocampus, and ACC of rats with bCCI injuries. However, SGK3 expression was downregulated in the spinal dorsal horn, DRG, hippocampus, and ACC of rats with bCCI injuries. Moreover, lncRNA CCAT1 overexpression could alleviate the pain thresholds and inhibited expression of SGK3 could rescue this effect. In conclusion, these results suggested the crucial roles of CCAT1 and SGK3 in the neuropathic pain.

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