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LncRNA NEAT1 promotes autophagy via regulating miR‐204/ATG3 and enhanced cell resistance to sorafenib in hepatocellular carcinoma
- Source :
- Journal of Cellular Physiology. 235:3402-3413
- Publication Year :
- 2019
- Publisher :
- Wiley, 2019.
-
Abstract
- Long noncoding RNAs (lncRNAs) has been acknowledged in tumorigenesis gradually because of the great importance in different cancers. LncRNA nuclear enriched abundant transcript 1 (NEAT1) is a novel lncRNA and has been reported to promote multiple cancer progression. However, the biological roles of NEAT1 in hepatocellular carcinoma (HCC) is not cleared nowadays. In the present research, the level of NEAT1 was found to be upregulated in HCC by The Cancer Genome Atlas. In addition, NEAT1 expression is negatively correlated with the survival rate in HCC. Further investigation revealed that NEAT1 upregulation inhibited sorafenib efficacy and promoted autophagy. We found that NEAT1 could be a sponge for microRNA-204 (miR-204) and inhibits its level to upregulate ATG3 expression. In addition to the above, we demonstrated that miR-204 mimics also attenuated tumor autophagy. And rescue assays demonstrated that NEAT1 promotes HCC autophagy through modulating miR-204/ATG3 pathway. Collectively, this study first demonstrated that a novel NEAT1/miR-204/ATG3 signaling regulates HCC progression.
- Subjects :
- 0301 basic medicine
Sorafenib
Carcinoma, Hepatocellular
Carcinogenesis
Physiology
Clinical Biochemistry
Autophagy-Related Proteins
Biology
medicine.disease_cause
Cell resistance
03 medical and health sciences
0302 clinical medicine
Downregulation and upregulation
Cell Line, Tumor
microRNA
Autophagy
medicine
Humans
Survival rate
Liver Neoplasms
Hep G2 Cells
Cell Biology
medicine.disease
digestive system diseases
Gene Expression Regulation, Neoplastic
MicroRNAs
030104 developmental biology
Drug Resistance, Neoplasm
030220 oncology & carcinogenesis
Hepatocellular carcinoma
Ubiquitin-Conjugating Enzymes
Cancer research
RNA, Long Noncoding
medicine.drug
Subjects
Details
- ISSN :
- 10974652 and 00219541
- Volume :
- 235
- Database :
- OpenAIRE
- Journal :
- Journal of Cellular Physiology
- Accession number :
- edsair.doi.dedup.....4cd46a35019d4439f4d4294829de28d8
- Full Text :
- https://doi.org/10.1002/jcp.29230