scholarly journals RPS27A is a Poor Prognostic Predictor for Hepatocellular Carcinoma via Interacting with METTL3-Mediated RNA Modifications

2021 ◽  
Author(s):  
Huiying Liu ◽  
Jianjun Zhu ◽  
Xiaoxia Kou ◽  
Lingling Guo ◽  
Hongjuan Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Quantitative Pcr ◽  
Cell Lines ◽  
Disease Free Survival ◽  
Rna Modification ◽  
Ppi Network ◽  
Rna Modifications ◽  
Pcr Assay ◽  
Prognostic Predictor ◽  
Quantitative Pcr Assay

Abstract Background: Increasing evidence has pointed to the involvement of RNA modifications in the pathogenesis of human cancers. However, they are rarely studied in hepatocellular carcinoma (HCC). Method: We summarized multiple types of RNA modification-related genes (RMRGs) from public references, and identified differentially expressed RMRGs (DEGs) between HCC tissues and matched normal samples, where their genetic variation were then investigated. The potential hub genes in the protein-protein interaction (PPI) network constructed by co-expression genes of RMRGs were recognized and verified in METTL3-knockdown HCC cell lines by quantitative PCR assay.Results: Seventy-six RMRGs, including six writers, seven readers, and seven erasers, were collected, of which 34 were identified and validated as DEGs. YTHDC2 exhibited the highest mutation rate, while ADAT2 showed widespread deletions. High correlations were observed between the expressions of 34 RMRGs. The PPI network constructed by 1080 co-expression DEGs related to RNA regulations consisted of 513 nodes and 11557 edges, with RPS27A presented the most directed edges and maximum closeness centrality. Patients with high expression of RPS27A showed worse overall survival (P < 0.01) and disease-free survival (P = 0.019). Moreover, RPS27A was found upregulated on high-risk metastatic and recurrent HCC tissues. Quantitative PCR assay indicated that RPS27A was significantly decreased in cancer cell lines when METTL3 was knocked down. Conclusions: Remarkable differences were observed for RNA modifications between HCC and normal samples, and RPS27A could be a poor prognostic predictor for HCC via interacting with METTL3-mediated RNA modifications.

scholarly journals MicroRNA-367 directly targets PIK3R3 to inhibit proliferation and invasion of oral carcinoma cells

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Haitao Sun ◽  
Xiaodong Feng
Keyword(s):  
Quantitative Pcr ◽  
Cell Lines ◽  
Hepatocellular Cancer ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Pcr Assay ◽  
Protein Levels ◽  
Cancer Types ◽  
Proliferation And Invasion ◽  
Quantitative Pcr Assay

Abstract Recently, microRNA-367 (miR-367) has been reported to function as both tumor suppressor and oncogene in several cancer types, including gastric cancer, hepatocellular cancer and lung cancer. However, the biological function of miR-367 and its precise mechanisms in oral squamous cell carcinoma (OSCC) have not been well clarified. The aim of the present study was to study the roles of miR-367/PIK3R3 axis in OSCC. The levels of PIK3R3 and miR-367 were detected by quantitative PCR assay in OSCC tissues and cell lines. Moreover, the biological roles of miR-367 and PIK3R3 in OSCC cells were assessed by cell proliferation and invasion. The mRNA and protein levels of PIK3R3 were determined by using quantitative PCR and Western blotting assays. Luciferase assays were used to confirm that PIK3R3 was one target of miR-367. In the present study, the miR-367 level was dramatically reduced in OSCC tissues and cell lines, and the PIK3R3 expression was significantly enhanced. What’s more, the PIK3R3 expression was negatively related to the miR-367 level in OSCC tissues. Furthermore, up-regulation of miR-367 obviously restrained OSCC cells proliferation and invasion. We confirmed that miR-367 could directly target PIK3R3 by luciferase reporter assay. Besides, knockdown of PIK3R3 also could markedly inhibit the proliferation and invasion of OSCC cells. Finally, overexpression of miR-367 in OSCC cells partially reversed the promoted effects of PIK3R3 up-regulation. Overexpression of miR-367 restrained OSCC cells proliferation and invasion via regulation of PIK3R3.

scholarly journals LncRNA SNHG17 Contributes to Proliferation, Migration, and Poor Prognosis of Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yue Luo ◽  
Junhao Lin ◽  
Jiakang Zhang ◽  
Zhenghui Song ◽  
Dayong Zheng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Rna Sequencing ◽  
Expression Pattern ◽  
Cell Lines ◽  
Disease Free Survival ◽  
Loss Of Function ◽  
Poor Overall Survival ◽  
Apoptotic Pathway ◽  
Qrt Pcr

Long noncoding RNAs (lncRNAs) have been substantially reported to have critical roles in regulating tumorigenesis in recent years. However, the expression pattern and biological function of SNHG17 in hepatocellular carcinoma (HCC) remain unclear. Bioinformatics analysis and qRT-PCR were performed to detect the expression pattern of SNHG17 in HCC tissues, adjacent nontumorous tissues, and cell lines. The effect of SNHG17 on proliferation, migration, and apoptosis of HCC was investigated by knockdown and overexpressing SNHG17 in HCC cell lines. RNA sequencing was utilized to explore the underlying mechanism. Utilizing publicly available TCGA-LIHC, GSE102079 HCC datasets, and qRT-PCR, we found SNHG17 was significantly upregulated in HCC tissues and cell lines and was notably associated with larger tumor size, poorly differentiation, presence of vascular invasion, and advanced TNM stage. Furthermore, gain- and loss-of-function studies demonstrated that SNHG17 promoted cell proliferation and migration and inhibited apoptosis of HCC. By employing RNA sequencing, we found knockdown of SNHG17 caused 1037 differentially expressed genes, highly enriched in several pathways, including metabolic, PI3K-Akt, cell adhesion, regulation of cell proliferation, and apoptotic pathway; among them, 92 were overlapped with SNHG17-related genes in the TCGA-LIHC dataset. Furthermore, ERH, TBCA, TDO2, and PDK4 were successfully validated and found significantly dysregulated in HCC tissues. Moreover, HCC patients with higher SNHG17 expression had a relatively poor overall survival and disease-free survival, and ERH and PDK4 also played a marked role in the prognosis of HCC. Broadly, our findings illustrate that SNHG17 acts as a noncoding oncogene in HCC progression, suggesting its potential value as a novel target for HCC therapy.

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