Overexpression of m 7 G writers METTL1 and BUD23 confers oncogenicity in kidney renal clear cell carcinoma

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Hauptverfasser: Anni Su, Jessica Tieng, Xueying S Xu, Richard P Tan, Yuchen Feng, Justin J‐L Wong
Format: Artículo Open Access
Veröffentlicht: Wiley 2025
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author Anni Su
Jessica Tieng
Xueying S Xu
Richard P Tan
Yuchen Feng
Justin J‐L Wong
author_facet Anni Su
Jessica Tieng
Xueying S Xu
Richard P Tan
Yuchen Feng
Justin J‐L Wong
Anni Su
Jessica Tieng
Xueying S Xu
Richard P Tan
Yuchen Feng
Justin J‐L Wong
collection Wiley Open Access
contents Overexpression of m 7 G writers METTL1 and BUD23 confers oncogenicity in kidney renal clear cell carcinoma Anni Su Jessica Tieng Xueying S Xu Richard P Tan Yuchen Feng Justin J‐L Wong The Journal of Pathology Abstract Emerging evidence shows that N7‐methylguanosine (m 7 G) modification and its writers contribute to the development of diverse cancers. However, the role of m 7 G writers in kidney renal clear cell carcinoma (KIRC) remains unclear. In this study we show that the catalytic components of m 7 G writers, METTL1 and BUD23, are overexpressed in advanced KIRC and are associated with worse overall survival. Knockdown of METTL1 or BUD23 inhibited cell proliferation, colony formation, and migration in KIRC cell lines, indicating their oncogenic role in KIRC. Furthermore, we observed that METTL1 and BUD23 expression was negatively correlated with the expression of key tumor suppressor genes commonly dysregulated in KIRC. We observed METTL1‐mediated m 7 G methylation in mRNAs expressed by these tumor suppressor genes, indicating that METTL1 may regulate these genes via m 7 G modification. Overall, our study highlights the oncogenic role of METTL1 and BUD23 in KIRC and their potential as prognostic biomarkers and therapeutic targets in KIRC. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. 10.1002/path.6453 http://creativecommons.org/licenses/by/4.0/
doi_str_mv 10.1002/path.6453
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institution Wiley Open Access
license_str_mv http://creativecommons.org/licenses/by/4.0/
publishDate 2025
publisher Wiley
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spellingShingle Overexpression of m 7 G writers METTL1 and BUD23 confers oncogenicity in kidney renal clear cell carcinoma
Anni Su
Jessica Tieng
Xueying S Xu
Richard P Tan
Yuchen Feng
Justin J‐L Wong
The Journal of Pathology
Overexpression of m 7 G writers METTL1 and BUD23 confers oncogenicity in kidney renal clear cell carcinoma Anni Su Jessica Tieng Xueying S Xu Richard P Tan Yuchen Feng Justin J‐L Wong The Journal of Pathology Abstract Emerging evidence shows that N7‐methylguanosine (m 7 G) modification and its writers contribute to the development of diverse cancers. However, the role of m 7 G writers in kidney renal clear cell carcinoma (KIRC) remains unclear. In this study we show that the catalytic components of m 7 G writers, METTL1 and BUD23, are overexpressed in advanced KIRC and are associated with worse overall survival. Knockdown of METTL1 or BUD23 inhibited cell proliferation, colony formation, and migration in KIRC cell lines, indicating their oncogenic role in KIRC. Furthermore, we observed that METTL1 and BUD23 expression was negatively correlated with the expression of key tumor suppressor genes commonly dysregulated in KIRC. We observed METTL1‐mediated m 7 G methylation in mRNAs expressed by these tumor suppressor genes, indicating that METTL1 may regulate these genes via m 7 G modification. Overall, our study highlights the oncogenic role of METTL1 and BUD23 in KIRC and their potential as prognostic biomarkers and therapeutic targets in KIRC. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. 10.1002/path.6453 http://creativecommons.org/licenses/by/4.0/
title Overexpression of m 7 G writers METTL1 and BUD23 confers oncogenicity in kidney renal clear cell carcinoma
topic The Journal of Pathology
url https://pathsocjournals.onlinelibrary.wiley.com/doi/10.1002/path.6453