scholarly journals Long Noncoding RNA FOXP4-AS1 Predicts Unfavourable Prognosis and Regulates Proliferation and Invasion in Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jingchen Liang ◽  
Duo Wang ◽  
Guanhua Qiu ◽  
Xiaoqi Zhu ◽  
Junjie Liu ◽  
...  

Background. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer that has a high level of morbidity and mortality. Long noncoding RNA (lncRNA) is a novel regulatory factor of tumour proliferation, apoptosis, and metastasis. Our previous studies indicated that lncRNA FOXP4-AS1 is a functional oncogene in HCC; thus, this study is aimed at further evaluating the clinical and biological function of FOXP4-AS1 in HCC. Material and Methods. First, we detected the expression of FOXP4-AS1 in HCC tissues and paracarcinoma normal tissues by qRT-PCR. Second, the prognostic effects of FOXP4-AS1 in patients with HCC were analysed in a training group and a verification group. Subsequently, to investigate the biological effects of FOXP4-AS1 on HCC cells, downexpression tests were further conducted. Results. The expression of FOXP4-AS1 was higher in HCC tissues than adjacent nontumourous tissues, whereas the low expression of FOXP4-AS1 was correlated with optimistic treatment outcomes, which suggested that FOXP4-AS1 may be an independent prognostic biomarker for HCC. Moreover, the downregulation of FOXP4-AS1 significantly reduced the cell proliferation and clonal abilities and inhibited the invasion, migration, and angiogenesis of hepatoma cells ( P < 0.05 ). Conclusion. These results revealed the clinical significance and biological function of FOXP4-AS1 in HCC development, which may provide a new direction for finding therapeutic targets and potential prognostic biomarkers of HCC.

2020 ◽  
Vol 98 (6) ◽  
pp. 709-718
Author(s):  
Qiang Liu ◽  
She-Jiao Dai ◽  
Lei Dong ◽  
Hong Li

Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related deaths worldwide, especially in developing countries. Although advances in surgical procedures and targeted medicine have improved the overall survival of patients with HCC, the prognosis is poor. Hence, there is a need to identify novel therapeutic targets for HCC. Here, we report that the expression of RP11-909N17.2, a novel, long, noncoding RNA (lncRNA), is dysregulated in patients with HCC and cell lines. Additionally, this study demonstrated that RP11-909N17.2 facilitates the proliferation and invasion of HCC cells by binding to miRNA-767-3p, a tumor-suppressive microRNA (miRNA). Small integral membrane protein 7 (SMIM7) was identified as the downstream target of miRNA-767-3p. The expression of SMIM7 was upregulated in HCC clinical samples and cell lines. Moreover, SMIM7 was involved in the proliferation and invasion of HCC cells. Furthermore, SMIM7 inhibited the apoptosis of HCC cells, which indicated the oncogenic role of SMIM7 in HCC. The findings of this study suggest that the lncRNA–miRNA–mRNA regulatory axis, which regulates the pathogenesis of HCC, can be a potential novel diagnostic and therapeutic target for HCC.


2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Fushun Li ◽  
Xianghua Sun ◽  
Qing Liu ◽  
Xilu Liu ◽  
Jia Zhang

Purpose. Hepatocellular carcinoma (HCC) accounts for approximately ninety percent of primary liver cancer. This study attempted to investigate the effects of the long noncoding RNA MIR100HG (MIR100HG) in HCC and the underlying molecular mechanism. Materials and Methods. qRT-PCR was implemented to analyze the expression of MIR100HG, microRNA-146b-5p (miR-146b-5p), and Chromobox 6 (CBX6). The correlation between MIR100HG and clinicopathological features of HCC patients was assessed. Additionally, the effects of MIR100HG knockdown on HCC cell viability, migration, and invasion were explored. The interactions among MIR100HG, miR-146b-5p, and CBX6 were confirmed. Furthermore, rescue experiments were conducted to investigate whether MIR100HG knockdown modulates HCC cell behaviors through modulating the miR-146b-5p/CBX6 axis. Results. The expression of MIR100HG and CBX6 was enhanced, while miR-146b-5p was inhibited in HCC cells. High MIR100HG expression was positively associated with the TNM tumor stage and Edmondson-Steiner grading in HCC patients. MIR100HG knockdown considerably reduced the HCC cell viability, migration, and invasion. In addition, MIR100HG directly targeted miR-146b-5p, and miR-146b-5p directly targeted CBX6 in HCC cells. Moreover, miR-146b-5p suppression or CBX6 elevation evidently rescued the suppressed viability, migration, and invasion of HCC cells caused by MIR100HG knockdown. Conclusions. Knockdown of MIR100HG inhibited the viability, migration, and invasion of HCC cells by targeting the miR-146b-5p/CBX6 axis, offering a potential therapeutic target for HCC therapy.


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