English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Colorectal cancer (CRC) is one of the most common cancers around the world and endangers human health seriously. Liver metastasis is an important factor affecting the long-term prognosis of CRC and the specific mechanism of CRLM (colorectal cancer with liver metastasis) is not fully understood.  LZTS1  has been found dysregulated in many cancers, especially in CRC. Theories suggested that hypermethylation of the promoter regions of  LZTS1  was responsible for  LZTS1  abnormal expression in multiple malignant tumors. Although the role of  LZTS1  in CRC cell proliferation has been reported, its role in CRLM remains unclear. Numerous studies reported Long non-coding RNA (lncRNA) could regulate the gene expression level by regulating gene methylation status in many tumors. However, whether there were lncRNAs could change the methylation status of  LZTS1  or not in CRLM was unknown. In this study, we aimed to investigate whether there are lncRNAs can regulate the expression of  LZTS1  through affecting DNA methylation in CRLM. We found that upregulated  Lnc-LALC  in CRC was negatively correlated with  LZTS1  expression, and  Lnc-LALC  could regulate  LZTS1  expression in both mRNA and protein level in our study. Functionally,  Lnc-LALC  enhanced the CRC cells metastasis ability in vitro and vivo through inhibiting the expression of  LZTS1 . Furthermore, the precise mechanisms exploration showed that  lnc-LALC  could recruit DNA methyltransferases (DNMTs) to the  LZTS1  promoter by combining with Enhancer of zeste homolog 2(EZH2) and then altered the expression of  LZTS1  via DNMTs-mediated DNA methylation. Collectively, our data demonstrated the important role of  Lnc-LALC/ LZTS1  axis in CRLM development.

Long non-coding RNA Lnc-LALC facilitates colorectal cancer liver metastasis via epigenetically silencing LZTS1