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<p>This study investigates the role of Early Growth Response 1 (EGR1) in extranodal natural killer/T-cell lymphoma (ENKTL) and its correlation with PD-L1 expression. Analysis of 62 ENKTL patient samples revealed that high EGR1 expression was linked to PD-L1 positivity, the immune evasion-A subtype, and early-stage disease. Although EGR1 expression was not an independent prognostic factor for overall survival, patients with higher EGR1 levels showed a trend toward better outcomes. In ENKTL cell lines (YT, SNK6), EGR1 positively regulated LMP1 and PD-L1 expression. Knockdown of EGR1 reduced PD-L1 levels, decreased PTEN, increased AKT phosphorylation, and abrogated STAT3 phosphorylation. Conversely, EGR1 overexpression enhanced PD-L1. Treatment with the histone deacetylase inhibitor entinostat upregulated both EGR1 and PD-L1, but this effect was lost in EGR1-depleted cells, indicating EGR1’s necessity for HDAC inhibitor–induced PD-L1 expression. These findings reveal EGR1’s pivotal role in tumor immune modulation and highlight potential combination therapies targeting EGR1, epigenetic regulators, and PD-1/PD-L1 checkpoints.</p><p></p>

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Early growth response 1 as a key regulator of PD-L1 expression and immune evasion in extranodal NK/T-cell lymphoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月13日

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  • Ji Yun Lee,
  • Kui-Jin Kim,
  • Woochan Park,
  • Jeongmin Seo,
  • Minsu Kang,
  • Eun Hee Jung,
  • Sang-A Kim,
  • Koung Jin Suh,
  • Ji-Won Kim,
  • Se Hyun Kim,
  • Jeong-Ok Lee,
  • Jin Won Kim,
  • Yu Jung Kim,
  • Keun-Wook Lee,
  • Jee Hyun Kim,
  • Soo-Mee Bang,
  • Tae Min Kim,
  • Jin Ho Paik

摘要

This study investigates the role of Early Growth Response 1 (EGR1) in extranodal natural killer/T-cell lymphoma (ENKTL) and its correlation with PD-L1 expression. Analysis of 62 ENKTL patient samples revealed that high EGR1 expression was linked to PD-L1 positivity, the immune evasion-A subtype, and early-stage disease. Although EGR1 expression was not an independent prognostic factor for overall survival, patients with higher EGR1 levels showed a trend toward better outcomes. In ENKTL cell lines (YT, SNK6), EGR1 positively regulated LMP1 and PD-L1 expression. Knockdown of EGR1 reduced PD-L1 levels, decreased PTEN, increased AKT phosphorylation, and abrogated STAT3 phosphorylation. Conversely, EGR1 overexpression enhanced PD-L1. Treatment with the histone deacetylase inhibitor entinostat upregulated both EGR1 and PD-L1, but this effect was lost in EGR1-depleted cells, indicating EGR1’s necessity for HDAC inhibitor–induced PD-L1 expression. These findings reveal EGR1’s pivotal role in tumor immune modulation and highlight potential combination therapies targeting EGR1, epigenetic regulators, and PD-1/PD-L1 checkpoints.