Novel N6-methyladenosine (m6A) writer METTL16 promotes the cervical cancer tumorigenesis by targeting FTH1-dependent ferroptosis

Iron-dependent programmed cell death (known as ferroptosis) is closely linked to cervical cancer progression. Here, the present research identified that novel N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) writer methyltransferase-like 16 (METTL16) was a ferroptosis-related gene in cervical cancer, and more exploration was performed to investigate its function and mechanism. Results showed that METTL16 was elevated in the cervical cancer cells, and METTL16 functionally repressed the ferroptosis-related characteristic. Mechanistically, ferritin heavy chain 1 (FTH1) was identified as a direct target of METTL16 via the m<sup>6</sup>A-dependent manner. In vivo, METTL16 silencing repressed the cervical cancer tumor growth. Therefore, these findings revealed that novel m<sup>6</sup>A writer METTL16 promoted the cervical cancer tumorigenesis by targeting FTH1-dependent ferroptosis, which providing distinct insights for cervical cancer.

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Publication Details

Journal
Discover Oncology
Published
2026-01-20
DOI
https://doi.org/10.1007/s12672-026-04403-8
Primary Topic
RNA modifications and cancer
Type
article
Field-Weighted Citation Impact
0.00
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article

Novel N6-methyladenosine (m6A) writer METTL16 promotes the cervical cancer tumorigenesis by targeting FTH1-dependent ferroptosis

Caihong Li, Youzhen Luo, Qiaoling Gao, Lulu Wang
Discover Oncology
RNA modifications and cancer
article

Novel N6-methyladenosine (m6A) writer METTL16 promotes the cervical cancer tumorigenesis by targeting FTH1-dependent ferroptosis

Caihong Li, Youzhen Luo, Qiaoling Gao, Lulu Wang
article en

Abstract

Iron-dependent programmed cell death (known as ferroptosis) is closely linked to cervical cancer progression. Here, the present research identified that novel N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) writer methyltransferase-like 16 (METTL16) was a ferroptosis-related gene in cervical cancer, and more exploration was performed to investigate its function and mechanism. Results showed that METTL16 was elevated in the cervical cancer cells, and METTL16 functionally repressed the ferroptosis-related characteristic. Mechanistically, ferritin heavy chain 1 (FTH1) was identified as a direct target of METTL16 via the m<sup>6</sup>A-dependent manner. In vivo, METTL16 silencing repressed the cervical cancer tumor growth. Therefore, these findings revealed that novel m<sup>6</sup>A writer METTL16 promoted the cervical cancer tumorigenesis by targeting FTH1-dependent ferroptosis, which providing distinct insights for cervical cancer.

Discover OncologyVol. 17(1)
Yichang Central People's Hospital (CN)
Good health and well-being
Openalex Percentile: Top 84%
RNA modifications and cancer
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