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SHMT2 promotes the tumorigenesis of renal cell carcinoma by regulating the m6A modification of PPAT
Serine hydroxymethyltransferase 2 (SHMT2) is the first rate-limiting enzyme for serine/glycine biosynthesis and one carbon metabolism. Here, we explore the underlying mechanism of how SHMT2 functions in renal cell carcinoma (RCC) initiation. In this study, SHMT2 expression was assessed in RCC tissue...
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Published in: | Genomics (San Diego, Calif.) Calif.), 2022-07, Vol.114 (4), p.110424-110424, Article 110424 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Serine hydroxymethyltransferase 2 (SHMT2) is the first rate-limiting enzyme for serine/glycine biosynthesis and one carbon metabolism. Here, we explore the underlying mechanism of how SHMT2 functions in renal cell carcinoma (RCC) initiation.
In this study, SHMT2 expression was assessed in RCC tissues. In vitro experiments were performed to investigate the functional role of SHMT2. The detailed mechanisms of SHMT2-mediated PPAT were addressed.
Increased SHMT2 facilitated RCC cell proliferation by inducing the G1/S phase transition. And SHMT2 promoted the expression of PPAT. Mechanism dissection revealed that SHMT2 enhanced the m6A modification through the endogenous methyl donor SAM mediated by SHMT2 via serine/glycine one carbon metabolic networks. SHMT2-catalyzed serine/glycine conversion regulated PPAT expression in an m6A-IGF2BP2-dependent manner. SHMT2 promoted RCC cell proliferation by upregulating PPAT expression.
SHMT2 promotes RCC tumorigenesis by increasing PPAT expression. Thus, SHMT2 may be a novel potential therapeutic target for RCC.
•Increased SHMT2 predicts poor prognosis in RCC.•SHMT2 promotes the growth of RCC through upregulating PPAT.•SHMT2 facilitates the m6A modification via serine/glycine metabolic networks.•IGF2BP2 enhances the mRNA stability of PPAT.•SHMT2 maintains the rapid growth of RCC by increasing serine catabolism. |
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ISSN: | 0888-7543 1089-8646 |
DOI: | 10.1016/j.ygeno.2022.110424 |