RESUMO
The clinical significance of microRNA (miR)1365p in hepatocellular carcinoma (HCC) has not been verified. Therefore, in the current study, the authors aimed to explore miR1365p expression and its clinical significance in HCC, as well as to investigate its potential target genes function. The authors detected the levels of miR1365p in 101 pairs of HCC and paracancer tissues via reverse transcriptionquantitative polymerase chain reaction. Gene Expression Omnibus database and the Cancer Genome Atlas (TCGA) database were used to further verify the clinical significance of miR1365p expression in HCC. The target genes prediction analysis of miR1365p, natural language processing (NLP) analysis of HCC in PubMed and gene functional enrichment analysis were conducted. The miR1365p level was markedly downregulated in HCC tissue, compared to paranontumor tissue. MiR1365p expression decreased in HCC patients with metastasis (P=0.004), advance TNM stage (P<0.001), portal vein tumor embolus (P=0.007) and vasoinvasion (P=0.003), compared with those HCC patients with nonmetastasis, early TNM stage, nonportal vein tumor embolus and nonvasoinvasion, respectively. In the TCGA database, downregulated miR1365p was also observed in HCC tissue compared to normal liver tissue (P<0.001). There were 178 genes obtained from the overlap between predicted targets and NLP analysis. GO and KEGG pathway analyses revealed some significant pathways related to cancers. Downregulation of miR1365p may be responsible for the carcinogenesis and aggressiveness of HCC. miR1365p may act as an anticarcinoma miRNA, which is essential for HCC progression through the regulation of various signaling pathways. Thus, miR1365p interaction may provide a novel strategy for HCC treatment.
Assuntos
Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , MicroRNAs/genética , Interferência de RNA , Adulto , Idoso , Biomarcadores Tumorais , Biologia Computacional , Bases de Dados Genéticas , Feminino , Ontologia Genética , Redes Reguladoras de Genes , Humanos , Masculino , Pessoa de Meia-Idade , Anotação de Sequência Molecular , Gradação de Tumores , Metástase Neoplásica , Estadiamento de Neoplasias , Curva ROC , Transdução de SinaisRESUMO
BACKGROUND: To explore the expression of DcR3 protein and its clinicopathological significance in bladder urothelial carcinomas (BUC). MATERIALS AND METHODS: Immunohistochemistry was performed to detect the expression of DcR3, caspase-3, Bcl-2, VEGF, Ki-67, PCNA and P53 in 166 BUC and 56 normal bladder tissues. Western blotting was used to detect the expression of DcR3 in the supernatants of cultured BUC cells. RESULTS: Overexpression of DcR3 was found in BUC tissues and cell lines, with significant elevation as compared to normal bladder tissues (p<0.0001). Higher DcR3 expression was related to the status of invasion, lymph node metastasis and recurrence. Furthermore, DcR3 expression was negatively correlated with caspase-3 and positively associated with Bcl-2, VEGF, Ki-67 labeling index (LI), PCNA LI and P53 (all p<0.0001), respectively. CONCLUSIONS: DcR3 may play a crucial role as an oncogene in tumorigenesis, deterioration and progress of BUC via influencing related pathways of apoptosis, proliferation and angiogenesis. The detection of DcR3 protein in the formalin- fixed and paraffin-embedded samples could assist to predict in prognosis of BUC patients.