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Background <p>In the tumor microenvironment (TME), exhausted CD8( +) T cells exhibit the impaired cytotoxic ability and function as the predominant responder to immune checkpoint blockade.</p> Objective <p>To explored the role of ZNF92, a poorly characterized transcription factor, in the progression and immune response of lung adenocarcinoma (LUAD).</p> Results <p>In LUAD tumors and cells, ZNF92 expression was enhanced. Functionally, ZNF92 deficiency impaired in vitro LUAD cell proliferation, migration and invasion, as well as diminished the in vivo tumorigenicity of LUAD cells. Moreover, ZNF92 deficiency diminished the apoptosis of tumor-associated CD8( +) T cells and enhanced their viability in vitro. Mechanistically, ZNF92 could enhance PD-L1 transcription. PD-L1 re-expression reversed the regulatory impacts of ZNF92 deficiency on phenotypes of LUAD cells and tumor-associated CD8( +) T cells.</p> Conclusion <p>Our study establishes that ZNF92 works as an oncogenic driver in LUAD by promoting PD-L1 transcription. ZNF92 inhibition could potentially serve as a therapeutic strategy for LUAD.</p>

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The transcription factor ZNF92 suppresses CD8( +) T cell viability and promotes malignant progression in lung adenocarcinoma by elevating PD-L1 expression

  • 期刊论文

  • 发表日期：

    2025年1月2日

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  • Xueqin Liu,
  • Jinpeng Liu,
  • Wei Wan,
  • Lihong Guo,
  • Jie Zhang

摘要

Background

In the tumor microenvironment (TME), exhausted CD8( +) T cells exhibit the impaired cytotoxic ability and function as the predominant responder to immune checkpoint blockade.

Objective

To explored the role of ZNF92, a poorly characterized transcription factor, in the progression and immune response of lung adenocarcinoma (LUAD).

Results

In LUAD tumors and cells, ZNF92 expression was enhanced. Functionally, ZNF92 deficiency impaired in vitro LUAD cell proliferation, migration and invasion, as well as diminished the in vivo tumorigenicity of LUAD cells. Moreover, ZNF92 deficiency diminished the apoptosis of tumor-associated CD8( +) T cells and enhanced their viability in vitro. Mechanistically, ZNF92 could enhance PD-L1 transcription. PD-L1 re-expression reversed the regulatory impacts of ZNF92 deficiency on phenotypes of LUAD cells and tumor-associated CD8( +) T cells.

Conclusion

Our study establishes that ZNF92 works as an oncogenic driver in LUAD by promoting PD-L1 transcription. ZNF92 inhibition could potentially serve as a therapeutic strategy for LUAD.