期刊
JOURNAL OF CANCER
卷 11, 期 19, 页码 5612-5622出版社
IVYSPRING INT PUBL
DOI: 10.7150/jca.46097
关键词
ALKBH5; IGF1R; Endometrial cancer; Insulin signaling pathway; m(6)A modification
类别
资金
- Shanghai municipal medical and health discipline construction projects [2017ZZ02015]
- National Natural Science Foundation of China [81871167]
- Natural Science Foundation of ShangHai [18ZR1430000]
N6-methyladenosine (m(6)A) messenger RNA methylation play important role in cell proliferation and tumorigenicity of endometrial cancer, but the key mechanism is not fully clear. Here, we found that RNA demethylase ALKBH5 expression was significantly upregulated in endometrial cancer, ALKBH5 was then identified to positively regulate proliferation and invasion of endometrial cancer. Mechanistically, the m(6)A eraser ALKBH5 demethylated target transcripts IGF1R and enhanced IGF1R mRNA stability, consequently promoting IGF1R translation and activating IGF1R signaling pathway. Thus, we demonstrated that ALKBH5 promoted proliferation and invasion of endometrial cancer via erasing IGF1R m(6)A-modifications, which suggests a potential therapeutic target for endometrial cancer.
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