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. 2023 Aug 15;14(8):520. doi: 10.1038/s41419-023-06049-8

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 9 — A Kaplan–Meier analysis of the relation between NR_033928 expression and patients’ survival. B Kaplan–Meier analysis of the relation between GLS expression and patients’ survival. C Representative images of immunohistochemistry analysis of GLS, Ki-67 and c-caspase3 expression in xenografts transfected with sh-NR_033928 lentivirus. Scale bar = 100 μm. D A schematic diagram of NR_033928 functions in GC. NSUN2 mediated NR_033928 m5C methylation thereby improving NR_033928 expression. NR_033928 promoted GC progression by glutamine metabolic reprogramming. Mechanistically, NR_033928 functions as a scaffold to recruit HUR and IGF2BP3 and increased GLS expression.