Long noncoding RNA CMPK2 promotes colorectal cancer progression by activating the FUBP3-c-Myc axis

Long noncoding RNAs (lncRNAs) have been shown to play crucial roles in cancer long noncoding RNAs (lncRNAs) have been known to play crucial roles in cancer development and progression by regulating chromatin dynamics and gene expression. However, only a few lncRNAs with annotated functions in the pr...

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Vydané v:Oncogene Ročník 39; číslo 19; s. 3926 - 3938
Hlavní autori: Gao, Qingzu, Zhou, Rui, Meng, Yuan, Duan, Rongfei, Wu, Ling, Li, Rui, Deng, Fengliu, Lin, Chuang, Zhao, Liang
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England Nature Publishing Group 07.05.2020
Predmet:
Animals
c-Myc protein
Cancer
Cell cycle
Cell Movement - genetics
Cell proliferation
Cell Proliferation - genetics
Chromatin
Colorectal cancer
Colorectal carcinoma
Colorectal Neoplasms - genetics
Colorectal Neoplasms - pathology
Disease Progression
DNA-Binding Proteins - genetics
Gene expression
HCT116 Cells
Heterografts
Humans
Metastases
Mice
Myc protein
Proto-Oncogene Proteins c-myc - genetics
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
Signal Transduction - genetics
Therapeutic applications
Transcription
Transcription Factors - genetics
ISSN:0950-9232, 1476-5594, 1476-5594
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Popis
Shrnutí:Long noncoding RNAs (lncRNAs) have been shown to play crucial roles in cancer long noncoding RNAs (lncRNAs) have been known to play crucial roles in cancer development and progression by regulating chromatin dynamics and gene expression. However, only a few lncRNAs with annotated functions in the progression of colorectal cancer (CRC) have been identified to date. In the present study, the expression of lncCMPK2 was upregulated in CRC tissues and positively correlated with clinical stages and lymphatic metastasis. The overexpression of lncCMPK2 promoted the proliferation and cell cycle transition of CRC cells. Conversely, the silencing of lncCMPK2 restricted cell proliferation both in vitro and in vivo. lncCMPK2 was localized to the nucleus of CRC cells, bound to far upstream element binding protein 3 (FUBP3), and guided FUBP3 to the far upstream element (FUSE) of the c-Myc gene to activate transcription. lncCMPK2 also stabilized FUBP3. These results provide novel insights into the functional mechanism of lncCMPK2 in CRC progression and highlight its potential as a biomarker of advanced CRC and therapeutic target.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0950-9232
1476-5594
1476-5594
DOI:10.1038/s41388-020-1266-8