Long non-coding RNAs (lncRNAs) snaR is a newly identified lncRNA with known functionality only in colon cancer. Our study was carried out to investigate the involvement of lncRNA snaR in human papillomaviruses (HPV)-negative cervical squamous cell carcinoma (CSCC). In the present study, plasma levels of lncRNA snaR in 108 patients with HPV-negative CSCC at stage I and II, and 35 healthy female controls were detected by real-time quantitative PCR. ROC curve analysis was performed to evaluate the diagnostic value of lncRNA snaR for HPV-negative CSCC. All patients were subjected to surgical resection and followed-up for 5 years to record cancer recurrence. lncRNA snaR expression vectors were transfected into HPV-negative CSCC cells. Cell migration and invasion ability were evaluated by Transwell migration and invasion assay, respectively. Expression levels of TGF-β1 were determined by Western blot. It was observed that lncRNA snaR was down-regulated in HPV-negative CSCC patients comparing with healthy controls. Down-regulation of lncRNA snaR effectively distinguished HPV-negative CSCC patients from healthy controls. lncRNA snaR was further down-regulated in patients with distant recurrence (DR) but not in patients with local-recurrence or without recurrence. lncRNA snaR overexpression decreased TGF-β1 expression in CSCC cells, while exogenous TGF-β1 treatment showed no significant effects on lncRNA snaR expression. lncRNA snaR overexpression inhibited cancer cell migration and invasion, while TGF-β1 treatment attenuated the inhibitory effect of lncRNA snaR overexpression on cancer cell migration and invasion. We therefore conclude that down-regulation of lncRNA snaR may induce postoperative DR of HPV-negative CSCC possibly through the interactions with TGF-β1.

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BackgroundThe duration of postsurgical pain is closely correlated with perioperative stress. Most patients suffer short-term sleep disorder/deprivation before and/or after surgery, which leads to extended postsurgical pain by an undetermined mechanism. The paraventricular thalamus (PVT) is a critical area that contributes to the regulation of feeding, awakening, and emotional states. However, whether the middle PVT is involved in postoperative pain or the extension of postoperative pain caused by perioperative sleep deprivation has not yet been investigated.MethodsWe established a model of postoperative pain by plantar incision with perioperative rapid eye movement sleep deprivation (REMSD) 6 h/day for 3 consecutive days in mice. The excitability of the CaMKIIα+ neurons in the middle PVT (mPVTCaMKIIα) was detected by immunofluorescence and fiber photometry. The activation/inhibition of mPVTCaMKIIα neurons was conducted by chemogenetics.ResultsREMSD prolonged the duration of postsurgical pain and increased the excitability of mPVTCaMKIIα neurons. In addition, mPVTCaMKIIα neurons showed increased excitability in response to nociceptive stimuli or painful conditions. However, REMSD did not delay postsurgical pain recovery following the ablation of CaMKIIα neurons in the mPVT. The activation of mPVTCaMKIIα neurons prolonged the duration of postsurgical pain and elicited anxiety-like behaviors. In contrast, inhibition of mPVTCaMKIIα neurons reduced the postsurgical pain after REMSD.ConclusionOur data revealed that the CaMKIIα neurons in the mPVT are involved in the extension of the postsurgical pain duration induced by REMSD, and represented a novel potential target to treat postoperative pain induced by REMSD.