Open AccessMETTL3‐mediated m6A methylation of ASPM drives hepatocellular carcinoma cells growth and metastasis
Author(s) -
Wang An,
Chen Xiaofeng,
Li Dongen,
Yang Liang,
Jiang Jianshuai
Publication year - 2021
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23931
Subject(s) - gene knockdown , gene silencing , biology , cancer research , hepatocellular carcinoma , microbiology and biotechnology , downregulation and upregulation , gene , genetics
Background Abnormal spindle‐like microcephaly (ASPM) has been proved to participate in tumor progression. However, the underlying mechanism of ASPM in liver hepatocellular carcinoma (LIHC) remains elusive. Methods The mRNA and protein expression were determined using Western blot and qRT‐PCR, and the capacities of cells proliferation, migration, and invasion were evaluated by CCK‐8, colony formation, wound healing, and transwell. MeRIP was performed to validate the interaction between ASPM and methyltransferase‐like 3 (METTL3). Results Herein, we found that ASPM was significantly upregulated in LIHC, and the high expression of ASPM was associated with poor LIHC prognosis. Furthermore, ASPM knockdown could suppress LIHC cells proliferation, migration, and invasion, while ASPM overexpression exerted reverse effect. Mechanistically, we revealed that the N6‐methyladenosine (m6A) modification of ASPM mRNA mediated by METTL3 promoted its expression in LIHC. More importantly, silencing METTL3 suppressed LIHC cells proliferation, migration, and invasion, which could be retained by ASPM overexpression. Conclusion Collectively, our findings suggested that METTL3/ASPM axis could serve as a novel promising therapeutic candidate for LIHC.