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Updated: Jun 10, 2025
07:49
Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
Published on: March 17, 2023
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The methionine cycle and its cancer implications.
Valentina Tassinari1, Wei Jia2, Wen-Lian Chen3
1Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy.
Oncogene
|October 11, 2024
Summary
Methionine metabolism impacts cancer by regulating S-adenosylmethionine (SAM) and gene expression. Inhibiting NR4A2 with Celecoxib shows potential for tumor growth control, offering new therapeutic avenues.
Area of Science:
- Biochemistry
- Oncology
- Molecular Biology
Background:
- Methionine is essential for sulfur metabolism and links to the folate cycle, forming one-carbon metabolism.
- One-carbon metabolism regulates S-adenosylmethionine (SAM), vital for cellular processes.
- Altered methionine metabolism is implicated in tumor growth and progression.
Purpose of the Study:
- To investigate the role of methionine metabolism in cancer development.
- To explore the regulatory mechanisms of SAM in tumor cells.
- To evaluate the therapeutic potential of targeting NR4A2.
Main Methods:
- Analysis of methionine and folate cycles.
- Assessment of SAM levels and their regulation.
- Investigation of NR4A2 mRNA methylation and its effect on proliferation.
- Evaluation of Celecoxib as an NR4A2 inhibitor in a cancer model.
Main Results:
- Methionine metabolism is critical for tumor growth, polyamine synthesis, and SAM regulation.
- NR4A2 mRNA methylation by SAM influences esophageal carcinoma proliferation.
- Celecoxib, an NR4A2 inhibitor, demonstrated potential in inhibiting tumor growth.
- Formaldehyde influences SAM levels and one-carbon metabolism, impacting cancer progression.
Conclusions:
- Methionine metabolism plays a significant role in cancer progression through SAM regulation and epigenetic modifications.
- Targeting NR4A2 presents a potential therapeutic strategy for esophageal carcinoma.
- Endogenous and exogenous formaldehyde can impact cancer development via one-carbon metabolism.
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