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To Wnt or Lose: The Missing Non-Coding Linc in Colorectal Cancer

期刊

出版社

MDPI
DOI: 10.3390/ijms18092003

关键词

Wnt; long non-coding RNA; CCAT1; CCAT2; PVT1; H19

资金

  1. National Institutes of Health (NIH/NCATS) through NIH Common Fund, Office of Strategic Coordination (OSC) [UH3TR00943-01]
  2. NIH/NCI [1 R01 CA182905-01]
  3. UPR/MDACC [U54]
  4. Team DOD grant [CA160445P1]
  5. Ladies Leukemia League grant
  6. CLL Moonshot Flagship project
  7. SINF
  8. Austrian Science Funds [J3389-B23]
  9. Estate of C. G. Johnson
  10. CDMRP [917395, CA160445P1] Funding Source: Federal RePORTER

向作者/读者索取更多资源

Colorectal cancer (CRC) is the third most frequent cancer and one of the leading causes for cancer-related mortality. Aberrant activation of the Wnt signaling is an essential initiating factor in colon carcinogenesis, and a driving force of CRC progression. Recently, long non-coding RNAs (lncRNAs) have emerged as significant players in CRC pathogenesis through diversified mechanisms. Although both Wnt signaling and lncRNAs represent interesting research areas for CRC, an effort of directly connecting these two areas is lacking. To fill in the knowledge gap, we focus on the reported findings of lncRNAs that regulate Wnt signaling or essential Wnt signaling targets. These include several newly discovered lncRNAs originated from the amplified cancer-associated chromosome 8q24 region that surrounds the essential Wnt target MYC gene, lncRNAs reported to be involved in CRC stem cells, and several individual lncRNAs connected to Wnt signaling through other mechanisms. This review will provide essential information that assists in understanding the missing link of lncRNAs to the classical Wnt signaling in CRC.

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