scholarly journals Down-regulation of lncRNA-NEF indicates poor prognosis in intrahepatic cholangiocarcinoma

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Zhanqiang Liang ◽  
Bingshuai Zhu ◽  
Dongdong Meng ◽  
Xiwen Shen ◽  
Xuemin Li ◽  
...  

Abstract LncRNA-NEF is a tumor suppressor lncRNA in liver cancer. The present study aimed to investigate the role of lncRNA-NEF in intrahepatic cholangiocarcinoma (IHCC), which is second most common type of primary cancer of the hepatobiliary system that causes high mortality rate. In the present study we found that lncRNA-NEF was down-regulated, while Runt-related transcription factor 1 (RUNX1) was up-regulated in tumor tissues than in adjacent healthy tissues of IHCC patients. Expression levels of lncRNA-NEF and RUNX1 were significantly and reversely correlated in tumor tissues but not in adjacent healthy tissues. Plasma levels of lncRNA-NEF were significantly lower in IHCC patients than in healthy controls. Down-regulation of lncRNA-NEF effectively distinguished stage I and II IHCC patients from healthy controls. Patients were followed up for 5 years, patients with high plasma levels of lncRNA-NEF showed significantly better survival conditions compared with patients with low expression levels of lncRNA-NEF. LncRNA-NEF overexpression led to inhibited expression of RUNX1 in cells of IHCC cell lines and inhibited cancer cell migration and invasion. In contrast, RUNX1 overexpression showed no significant effects on lncRNA-NEF expression, but attenuated the effects of lncRNA-NEF overexpression on cancer cell migration and invasion. We therefore concluded that lncRNA-NEF participated in IHCC possibly by interacting with RUNX1.

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Wei Li ◽  
Xingyu Wu ◽  
Wensheng She

Abstract Up-regulation of lncRNA POU3F3 has been observed in esophageal squamous cell carcinomas, while its expression pattern and functionality in other human disease is unknown. Our study showed that plasma levels of lncRNA POU3F3 and TGF-β1 (transforming growth factor-β) were both increased in nasopharyngeal carcinoma patients than in healthy controls. Plasma levels of lncRNA POU3F3 were not affected by the diameter of primary tumors but increased in patients with tumor metastasis. Plasma levels of lncRNA POU3F3 and TGF-β1 were positively correlated only in nasopharyngeal carcinoma patients but not in healthy controls. Follow-up study showed that high plasma levels of lncRNA POU3F3 were significantly correlated with poor overall survival. LncRNA POU3F3 overexpression and exogenous TGF-β1 treatment led to promoted, while TGF-β1 inhibitor led to inhibited migration and invasion of nasopharyngeal carcinoma cells. TGF-β1 inhibitor partially rescued the inhibited cancer cell migration and invasion caused by lncRNA POU3F3 overexpression. LncRNA POU3F3 overexpression led to down-regulated TGF-β1 expression, while exogenous TGF-β1 and TGF-β1 inhibitor treatment did not significantly change the expression level of lncRNA POU3F3. Therefore, lncRNA POU3F3 may promote cancer cell migration and invasion in nasopharyngeal carcinoma by up-regulating TGF-β1.


2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Zhenli Zheng ◽  
Yuqing Gao

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.


2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Shouzhang Yang ◽  
Huajie Cai ◽  
Bingren Hu ◽  
Jinfu Tu

Abstract In the present study, we investigated the role of lncRNA SAMMSON in hepatocellular carcinoma (HCC). We found that SAMMSON was up-regulated in HCC tissues, and patients with high levels of SAMMSON in HCC tissues had significantly lower overall rate within 5 years after admission. miR-9-3p was down-regulated in HCC tissues and inversely correlated with SAMMSON. SAMMSON expression was not significantly affected by HBV and HCV infections in HCC patients. In HCC cells, SAMMSON overexpression resulted in down-regulated miR-9-3p expression, while miR-9-3p overexpression caused no significant changes in expression levels of SAMMSON. SAMMSON overexpression led to increased, while miR-9-3p overexpression resulted in decreased migration and invasion rates of HCC cells. Therefore, SAMMSON negatively regulated miR-9-3p in HCC cells to promote cancer cell migration and invasion.


2021 ◽  
Author(s):  
Thanawat Suwatthanarak ◽  
Masayoshi Tanaka ◽  
Yoshitaka Miyamoto ◽  
Kenji Miyado ◽  
Mina Okochi

A CD9-binding peptide (RSHRLRLH), screened from EWI-2, was characterized, and its inhibition effect on cancer-cell migration and invasion was demonstrated.


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