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METTL3 inhibition promotes radiosensitivity in hepatocellular carcinoma through regulation of SLC7A11 expression
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METTL3 inhibition promotes radiosensitivity in hepatocellular carcinoma through regulation of SLC7A11 expression
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Journal Article
METTL3 inhibition promotes radiosensitivity in hepatocellular carcinoma through regulation of SLC7A11 expression
2025
Overview
Radiotherapy is one of the main treatment modalities for advanced hepatocellular carcinoma (HCC). Ferroptosis has been shown to promote the radiosensitivity of HCC cells, but it remains unclear whether epigenetic regulations function in this process. In this study, we found that the overexpression of METTL3 was associated with poor prognosis. Knockdown of METTL3 promoted radiosensitivity of HCC by inducing ferroptosis. Mechanistically, METTL3 targeted adenine (+1795) on the SLC7A11 mRNA, and the m
6
A reader IGF2BP2 promoted SLC7A11 mRNA stability by recognizing and binding to the m
6
A site. Additionally, METTL3 decreased the ubiquitination of SLC7A11 protein through the m
6
A/YTHDF2/SOCS2 axis. Furthermore, in vivo studies showed that HCC models with low METTL3/IGF2BP2 expression have higher radiosensitivity. In conclusion, our study suggests that METTL3 regulates the stability of SLC7A11 mRNA in an m
6
A/IGF2BP2-dependent manner and the ubiquitination of SLC7A11 protein through the m
6
A/YTHDF2/SOCS2 pathway, both of which require the m
6
A methyltransferase activity of METTL3. METTL3 or IGF2BP2 may be promising targets for radiotherapy of HCC.
Highlights
METTL3 contributed to the resistance to radiation by regulating the expression of SLC7A11 in HCC cells.
METTL3 maintained the mRNA stability of SLC7A11 in an m
6
A/IGF2BP2-dependent manner, via the binding of IGF2BP2 with the m6A site (+1795) of SLC7A11 mRNA.
METTL3 decreased the ubiquitination of SLC7A11 protein through the m
6
A/YTHDF2/SOCS2 axis.
Knockdown of METTL3/IGF2BP2 improved the radiosensitivity of HCC.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ 13/109
/ 13/89
/ 38/1
/ 38/77
/ 64/60
/ 82/80
/ Amino Acid Transport System y+ - genetics
/ Amino Acid Transport System y+ - metabolism
/ Animals
/ Biomedical and Life Sciences
/ Carcinoma, Hepatocellular - genetics
/ Carcinoma, Hepatocellular - metabolism
/ Carcinoma, Hepatocellular - pathology
/ Carcinoma, Hepatocellular - radiotherapy
/ Female
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Liver Neoplasms - metabolism
/ Liver Neoplasms - radiotherapy
/ Male
/ Methyltransferases - antagonists & inhibitors
/ Methyltransferases - genetics
/ Methyltransferases - metabolism
/ Mice
/ Proteins
/ Radiation Tolerance - genetics
/ RNA-Binding Proteins - genetics
