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<p>Carnitine palmitoyltransferase 1A (CPT1A), a succinylating enzyme, is highly expressed in various malignant tumors and promotes tumor progression. Succinylation is a posttranslational modification that has been reported in various diseases, but its role in NK/T-Cell lymphoma nasal type (ENKTL-NT) remains underexplored. In this study, bioinformatics analysis showed that glycolytic is a major metabolic pathway in ENKTL-NT as the expression of many glycolytic related kinases are increased. CPT1A probably mediates glycolytic process, as indicated by GO-enrichment analysis. Studies showed that CPT1A was upregulated in ENKTL-NT tissues, and that high CPT1A expression was associated with poor prognosis of ENKTL-NT. CPT1A promoted the proliferation, colony formation, invasion and glycolytic process of ENKTL-NT cells and suppresses apoptosis. Mechanistically, CPT1A promotes succinylation of LDHA at lysine 318 (K318), which increase the protein stability and the final protein level of LDHA. Both knockdown and mutation (K318R) of LDHA abolished the cancer-promoting effects of CPT1A in ENKTL-NT. In all, this study reveals the mechanism underlying the cancer-promoting effects of CPT1A via inducing LDHA succinylation and metabolic reprogramming in ENKTL-NT. These findings might provide potential targets for the diagnosis or therapy of ENKTL-NT.</p>

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CPT1A mediates succinylation of LDHA at K318 site promoteing metabolic reprogramming in NK/T-cell lymphoma nasal type

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月11日

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  • Hao Tian,
  • Yi Ge,
  • Jianjun Yu,
  • Xing Chen,
  • Honghan Wang,
  • Xu Cai,
  • Zhenfeng Shan,
  • Liang Zuo,
  • Yan Liu

摘要

Carnitine palmitoyltransferase 1A (CPT1A), a succinylating enzyme, is highly expressed in various malignant tumors and promotes tumor progression. Succinylation is a posttranslational modification that has been reported in various diseases, but its role in NK/T-Cell lymphoma nasal type (ENKTL-NT) remains underexplored. In this study, bioinformatics analysis showed that glycolytic is a major metabolic pathway in ENKTL-NT as the expression of many glycolytic related kinases are increased. CPT1A probably mediates glycolytic process, as indicated by GO-enrichment analysis. Studies showed that CPT1A was upregulated in ENKTL-NT tissues, and that high CPT1A expression was associated with poor prognosis of ENKTL-NT. CPT1A promoted the proliferation, colony formation, invasion and glycolytic process of ENKTL-NT cells and suppresses apoptosis. Mechanistically, CPT1A promotes succinylation of LDHA at lysine 318 (K318), which increase the protein stability and the final protein level of LDHA. Both knockdown and mutation (K318R) of LDHA abolished the cancer-promoting effects of CPT1A in ENKTL-NT. In all, this study reveals the mechanism underlying the cancer-promoting effects of CPT1A via inducing LDHA succinylation and metabolic reprogramming in ENKTL-NT. These findings might provide potential targets for the diagnosis or therapy of ENKTL-NT.