2. Academic Validation
  3. Long noncoding RNA CMPK2 promotes colorectal cancer progression by activating the FUBP3-c-Myc axis

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

  • Oncogene. 2020 May;39(19):3926-3938. doi: 10.1038/s41388-020-1266-8.
Qingzu Gao  # 1 2 3,  Rui Zhou  # 1 3,  Yuan Meng 1 4,  Rongfei Duan 5,  Ling Wu 1 3,  Rui Li 1 3,  Fengliu Deng 1 3,  Chuang Lin 1,  Liang Zhao 6 7
Affiliations

Affiliations

  • 1 Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
  • 2 Department of Pathology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.
  • 3 Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
  • 4 Department of Pathology, The Second People's Hospital of Longgang District, Shenzhen, China.
  • 5 Department of Endocrinology, The First Affiliated Hospital of Xinxiang Medical University, Guangzhou, China.
  • 6 Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China. liangsmu@foxmail.com.
  • 7 Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. liangsmu@foxmail.com.
  • # Contributed equally.
PMID: 32203166 DOI: 10.1038/s41388-020-1266-8
Abstract

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.

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