Abstract
Colorectal cancer (CRC) is a highly malignant tumor associated with poor prognosis, yet the molecular mechanisms are not fully understood. In this study, we showed that LYAR, a nucleolar protein, is expressed at a higher level in CRC tissue than in adjacent normal tissue and that LYAR expression is closely associated with distant CRC metastasis. LYAR not only significantly promotes the migration and invasion of CRC cells in vitro, but knockdown (KD) of LYAR in CRC cells also inhibits xenograft tumor metastasis in vivo. Microarray analysis of LYAR KD cells combined with a chromatin immunoprecipitation (ChIP) assay, gene reporter assay, and rescue experiment indicated that FSCN1 (encoding fascin actin-bundling protein 1 (Fascin-1)) serves as a novel key regulator of LYAR-promoted migration and invasion of CRC cells. Knockdown of FSCN1 significantly inhibits subcutaneous tumorigenesis of CRC cells and leads to the downregulation of FASN and SCD, genes encoding key enzymes in fatty acid synthesis. In summary, this study reveals a novel mechanism by which LYAR promotes tumor cell migration and invasion by upregulating FSCN1 expression and affecting fatty acid metabolism in CRC.
Highlights
Colorectal cancer (CRC) is the third most frequently diagnosed cancer, with 1.85 million new cases in 2018, and is the second most common cause of cancer-related mortality worldwide [IARC World Cancer Report 2020] [1]
High LYAR expression was significantly correlated with poor prognosis (Figure 1(b)), which was consistent with the survival curve analysis of CRC data from The Cancer Genome Atlas (TCGA) database (Figure S1)
These results indicate that LYAR is highly expressed in CRC tissues, metastatic tissues
Summary
Colorectal cancer (CRC) is the third most frequently diagnosed cancer, with 1.85 million new cases in 2018, and is the second most common cause of cancer-related mortality worldwide [IARC World Cancer Report 2020] [1]. Oxidative Medicine and Cellular Longevity and endothelium, enter the blood and lymph vessels, survive migration, and attach at a distant site, where tumor cells begin to proliferate, induce angiogenesis, evade apoptotic death, and form a new tumor [6, 7]. These distant settlements of tumor cells, metastases, are the cause of 90% of human cancer deaths [6, 8,9,10]. The molecular mechanism involved in the cascade of events during invasion and metastasis of CRC is still not fully understood
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
