4.6 Article

ALKBH5 regulates IGF1R expression to promote the Proliferation and Tumorigenicity of Endometrial Cancer

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

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资金

  1. Shanghai municipal medical and health discipline construction projects [2017ZZ02015]
  2. National Natural Science Foundation of China [81871167]
  3. Natural Science Foundation of ShangHai [18ZR1430000]

向作者/读者索取更多资源

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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