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<p>Lung cancer is the leading cause of cancer-related deaths globally, with tumour growth, invasion, and treatment response heavily influenced by the tumour microenvironment (TME). The TME promotes tumour progression by creating an immunosuppressive environment that hampers the body’s antitumour immune response, primarily through the Nuclear Factor Kappa B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3) pathways. These pathways contribute to chronic inflammation, immune evasion, and angiogenesis. Targeting the TME and its signalling pathways has shown potential to enhance treatment efficacy. STAT3, a key transcription factor in lung cancer, drives tumour growth and immune suppression via the mTOR and JAK pathways. Inhibiting these pathways can block STAT3 and slow cancer progression. Promising results have been observed with mTOR inhibitors like CC-115 and Vistusertib, especially when combined with immune checkpoint inhibitors, and with JAK inhibitors such as Ruxolitinib, AZD4205, and Filgotinib. These strategies represent a promising direction for lung cancer therapy. This review explores the intricate relationship between the TME and lung cancer, focussing on novel therapeutic approaches that target immune cells, signalling molecules, and fibroblasts within the TME to improve patient outcomes.</p> Graphical abstract <p>Overview of the lung TME, illustrating key cellular components, signalling pathways, and their roles in tumour proliferation, metastasis, immune evasion, and angiogenesis.</p>

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The role of the tumour microenvironment in lung cancer and its therapeutic implications

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月23日

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  • Devindi Thathsara Edirisinghe,
  • Jasleen Kaur,
  • Yue Qi Lee,
  • Huey Xin Lim,
  • Sharis Wan Ting Lo,
  • Sri Vishupriyaa,
  • Ee Wern Tan,
  • Rebecca Shin Yee Wong,
  • Bey Hing Goh

摘要

Lung cancer is the leading cause of cancer-related deaths globally, with tumour growth, invasion, and treatment response heavily influenced by the tumour microenvironment (TME). The TME promotes tumour progression by creating an immunosuppressive environment that hampers the body’s antitumour immune response, primarily through the Nuclear Factor Kappa B (NF-κB) and Signal Transducer and Activator of Transcription 3 (STAT3) pathways. These pathways contribute to chronic inflammation, immune evasion, and angiogenesis. Targeting the TME and its signalling pathways has shown potential to enhance treatment efficacy. STAT3, a key transcription factor in lung cancer, drives tumour growth and immune suppression via the mTOR and JAK pathways. Inhibiting these pathways can block STAT3 and slow cancer progression. Promising results have been observed with mTOR inhibitors like CC-115 and Vistusertib, especially when combined with immune checkpoint inhibitors, and with JAK inhibitors such as Ruxolitinib, AZD4205, and Filgotinib. These strategies represent a promising direction for lung cancer therapy. This review explores the intricate relationship between the TME and lung cancer, focussing on novel therapeutic approaches that target immune cells, signalling molecules, and fibroblasts within the TME to improve patient outcomes.

Graphical abstract

Overview of the lung TME, illustrating key cellular components, signalling pathways, and their roles in tumour proliferation, metastasis, immune evasion, and angiogenesis.