FTO mediated ERBB2 demethylation promotes tumor progression in esophageal squamous cell carcinoma cells

N 6 -methyladenosine (m 6 A) is the most prevalent and internal modification that occurs in the messenger RNAs of eukaryotes. However, knowledge of the impact of these modifications on gene expression regulation remains limited. By using the in vitro MeRIP-seq and RNA-seq assays, we discovered that...

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Bibliographic Details
Published in:Clinical & experimental metastasis 2022-08, Vol.39 (4), p.623-639
Main Authors: Zhao, Fangfang, Ge, Fangfang, Xie, Minghua, Li, Zhenyu, Zang, Chunbao, Kong, Lingsuo, Pu, Youguang, Zheng, Xucai, Tan, Yiao
Format: Article
Language:English
Subjects:
Biomedical and Life Sciences
Biomedicine
Cancer Research
Cell proliferation
Demethylation
ErbB-2 protein
Esophageal cancer
Eukaryotes
Gene expression
Gene regulation
Growth factors
Hematology
Hospitals
Kinases
Life sciences
Medicine
Metastases
Metastasis
N6-methyladenosine
Oncology
Plasmids
Proteins
Research Paper
Ribonucleic acid
RNA
Squamous cell carcinoma
Surgery
Surgical Oncology
Transcriptomes
Tumorigenesis
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Summary:N 6 -methyladenosine (m 6 A) is the most prevalent and internal modification that occurs in the messenger RNAs of eukaryotes. However, knowledge of the impact of these modifications on gene expression regulation remains limited. By using the in vitro MeRIP-seq and RNA-seq assays, we discovered that the mRNA demethylase FTO was significantly up-regulated in esophageal squamous cell carcinoma (ESCC) tissues and cells. Knockdown of FTO drastically suppressed the proliferation, migration, and invasion of ESCC cells. Furthermore, by using transcriptome-wide m 6 A-seq and RNA-seq assays, we identified ERBB2 is the target of FTO, which acts in concert in ESCC tumorigenesis and metastasis. Moreover, loss and gain functional studies suggested that the m 6 A reader YTHDF1 stabilizes ERBB2 mRNA via decoding the m 6 A modification. All these results uncovered a new signaling cascade, including FTO, YTHDF1, and ERBB2, which finely regulates the ESCC progression.
ISSN:0262-0898
1573-7276
DOI:10.1007/s10585-022-10169-4