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METTL14 suppresses proliferation and metastasis of colorectal cancer by down-regulating oncogenic long non-coding RNA XIST
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METTL14 suppresses proliferation and metastasis of colorectal cancer by down-regulating oncogenic long non-coding RNA XIST
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Journal Article
METTL14 suppresses proliferation and metastasis of colorectal cancer by down-regulating oncogenic long non-coding RNA XIST
2020
Overview
Background
N6-methyladenosine (m6A) is the most prevalent RNA epigenetic regulation in eukaryotic cells. However, understanding of m6A in colorectal cancer (CRC) is very limited. We designed this study to investigate the role of m6A in CRC.
Methods
Expression level of METTL14 was extracted from public database and tissue array to investigate the clinical relevance of METTL14 in CRC. Next, gain/loss of function experiment was used to define the role of METTL14 in the progression of CRC. Moreover, transcriptomic sequencing (RNA-seq) was applied to screen the potential targets of METTL14. The specific binding between METTL14 and presumed target was verified by RNA pull-down and RNA immunoprecipitation (RIP) assay. Furthermore, rescue experiment and methylated RNA immunoprecipitation (Me-RIP) were performed to uncover the mechanism.
Results
Clinically, loss of METTL14 correlated with unfavorable prognosis of CRC patients. Functionally, knockdown of METTL14 drastically enhanced proliferative and invasive ability of CRC cells in vitro and promoted tumorigenicity and metastasis in vivo. Mechanically, RNA-seq and Me-RIP identified lncRNA
XIST
as the downstream target of METTL14. Knockdown of METTL14 substantially abolished m6A level of
XIST
and augmented
XIST
expression. Moreover, we found that m6A-methylated
XIST
was recognized by YTHDF2, a m6A reader protein, to mediate the degradation of
XIST
. Consistently,
XIST
expression negatively correlated with METTL14 and YTHDF2 in CRC tissues.
Conclusion
Our findings highlight the function and prognostic value of METTL14 in CRC and extend the understanding of the importance of RNA epigenetics in cancer biology.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Biomarkers, Tumor - genetics
/ Biomarkers, Tumor - metabolism
/ Biomedical and Life Sciences
/ Cloning
/ Colorectal Neoplasms - genetics
/ Colorectal Neoplasms - metabolism
/ Colorectal Neoplasms - pathology
/ Female
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Liver Neoplasms - metabolism
/ m6A
/ Methyltransferases - genetics
/ Methyltransferases - metabolism
/ METTL14
/ Mice
/ Non-coding RNAs and RNA modifiers in cancer progression and cancer cells resistance to therapies
/ Oncology
/ Patients
/ Plasmids
/ Proteins
/ RNA
