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E2F1-induced lncRNA, EMSLR regulates lncRNA LncPRESS1
被引:10
|作者:
Priyanka, Priyanka
[1
]
Sharma, Madhur
[3
]
Das, Sanjeev
[1
]
Saxena, Sandeep
[1
,2
]
机构:
[1] Natl Inst Immunol, Aruna Asaf Ali Marg, New Delhi 110067, India
[2] JNU, New Delhi, India
[3] UDSC, New Delhi, India
关键词:
LONG NONCODING RNA;
GENOME REGULATION;
CELL-GROWTH;
C-MYC;
CHROMATIN;
PROLIFERATION;
CYCLIN;
METASTASIS;
EXPRESSION;
PROGNOSIS;
D O I:
10.1038/s41598-022-06154-2
中图分类号:
O [数理科学和化学];
P [天文学、地球科学];
Q [生物科学];
N [自然科学总论];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
E2F1 induces hundreds of protein-coding genes influencing diverse signaling pathways but much less is known about its non-coding RNA targets. For identifying E2F1-dependent oncogenic long non-coding RNAs (lncRNAs), we carried out genome-wide transcriptome analysis and discovered an lncRNA, EMSLR, which is induced both in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). EMSLR depletion blocks the cells in G1 phase and inhibits the clonogenic ability indicating that it is essential for the tumor-related phenotypes. We discovered that EMSLR represses the promoter activity of another lncRNA, LncPRESS1, which is located 6.9 kb upstream of EMSLR and they display an inverse expression pattern in lung cancer cell lines. Depletion of C-MYC results in downregulation of EMSLR and simultaneous upregulation of EMSLR target LncPRESS1, exemplifying how C-MYC and E2F1 signal transduction pathways control the network of lncRNA genes to modulate cell proliferation and differentiation.
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页数:16
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