LINC00244 suppresses cell growth and metastasis in hepatocellular carcinoma by downregulating programmed cell death ligand 1.
Zhijia SunChunyuan XueJiangbo LiHui ZhaoYimeng DuNan DuPublished in: Bioengineered (2022)
The role of programmed cell death ligand 1 (PD-L1) in suppressing antitumor immune responses has been widely reported, and recent studies showed that PD-L1 also plays an important role in epithelial-mesenchymal transition (EMT), determination of tumor cell phenotypes, metastasis, and drug resistance. Long non-coding RNAs (lncRNAs) are involved in a variety of epigenetic regulatory processes. The tumorigenesis and development of most cancers cannot be studied separately from their regulation by lncRNAs. To explore the epigenetic regulation of PD-L1, we identified an lncRNA, LINC00244, which reduced PD-L1 expression and predicted good clinical outcomes in hepatocellular carcinoma (HCC). LINC00244 inhibited the proliferation, invasion, and metastasis of HCC by downregulating PD-L1 expression. In addition, low LINC00244 expression activated epithelial-mesenchymal transition (EMT) pathways and facilitated the rapid growth and metastasis of HCC cells. Thus, LINC00244 is a potential therapeutic target for HCC.
Keyphrases
- long non coding rna
- epithelial mesenchymal transition
- poor prognosis
- signaling pathway
- induced apoptosis
- transforming growth factor
- long noncoding rna
- immune response
- single cell
- cell therapy
- dna methylation
- pi k akt
- stem cells
- network analysis
- high resolution
- dendritic cells
- climate change
- toll like receptor
- risk assessment
- cell death
- cell migration
- mass spectrometry
- solid phase extraction
- simultaneous determination