Evaluating the diagnostic and prognostic value of long non-coding RNA SNHG15 in pancreatic ductal adenocarcinoma.

OBJECTIVE: Long non-coding RNA SNHG15 (SNHG15) has been reported to play very important roles in the malignancy behaviors of various tumors, including pancreatic ductal adenocarcinoma (PDAC). However, its clinical significance in PDAC remains largely unclear. The aim of this study was to investigate whether the aberrant expression of SNHG15 can be used as potential prognostic and diagnostic markers of human PDAC. MATERIALS AND METHODS: TaqMan Real Time-PCR was performed to investigate the expression of SNHG15 in PDAC tissues and serum samples. Receiver operator characteristic (ROC) analysis was applied to obtain the diagnostic utility of SNHG15. Association between SNHG15 levels and clinicopathological factors was analyzed. Kaplan-Meier curves and multivariate Cox proportional models were used to study the impact on clinical outcome. RESULTS: SNHG15 levels were significantly up-regulated in both sera and tumors tissues from PDAC patients. ROC curve analysis revealed that SNHG15 may be a potential biomarker for differentiating PDAC tissues from normal pancreatic tissues, and the plasma levels of SNHG15 may be a potential biomarker for differentiating PDAC patients from healthy controls. Clinicopathologic analysis revealed that high SNHG15 expression was associated with tumor differentiation (p = 0.000), lymph node metastasis (p = 0.001) and tumor stage (p = 0.005). Furthermore, patients with high SNHG15 expression had a shorter overall survival compared with the low SNHG15 expression group (p = 0.003). Also, Cox multivariate analyses confirmed that SNHG15 expression was an independent prognostic factor in PDAC (p < 0.004). CONCLUSIONS: Our study firstly indicated the potential value of SNHG15 as an important biomarker for the diagnosis and prognosis prediction of PDAC.

Interleukin-27 augments the inhibitory effects of sorafenib on bladder cancer cells

Both sorafenib and interleukin-27 (IL-27) are antineoplastic drugs. This study aimed to investigate the synergistic effect of these two drugs on bladder cancer cells. HTB-9 and T24 cells were stimulated with IL-27 (50 ng/mL), sorafenib (2 μM) or the synergistic action of these two drugs. The cells without treatment acted as control. Cell proliferation, apoptosis and invasion were measured by bromodeoxyuridine assay, flow cytometry and modified Boyden chamber, respectively. Simultaneously, both modified Boyden chamber and scratch assay were used to assess cell migration. Finally, the phosphorylation levels of key kinases in the Akt/mechanistic target of rapamycin (mTOR)/mitogen-activated protein kinase (MAPK) pathway, and expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 were detected by western blot analysis. Stimulation with IL-27 or sorafenib repressed proliferation, migration and invasion but promoted apoptosis, and the effects were all enhanced by the combination of these two drugs in HTB-9 cells. The effect of the combined treatment on bladder cancer cells was verified in T24 cells. Additionally, the phosphorylation levels of AKT, mTOR and MAPK as well as the expression levels of MMP-2 and MMP-9 were all decreased by a single treatment of IL-27 or sorafenib, and further decreased by the combined treatment of these two drugs. The combination of IL-27 and sorafenib inhibited proliferation, migration and invasion and promoted apoptosis of bladder cancer cells compared with mono-drug treatment. Additionally, the AKT/mTOR/MAPK pathway might be implicated in the functional effects by down-regulations of MMP-2 and MMP-9.