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<p>Lung cancer (LC) primarily affects men and is the third most common cause of cancer-related death worldwide. Treatment for LC involves many phases, each with specific challenges arising from the characteristics of malignancy and the limitations of chemotherapy. GSK-3β, a serine/threonine kinase factor, is essential for several signals that control important cellular functions and a variety of diseases, including cancer. GSK-3β regulates transcription factors through phosphorylation, which in turn activates signaling pathways such as PI3K/AKT/mTOR, Wnt/β-catenin, and NF-κB. These signaling pathways might affect LC. Additionally, targeting GSK-3β offers a promising approach to overcoming drug resistance in cancer therapy. Inhibiting GSK-3β has been demonstrated to boost chemotherapy sensitivity, making cancer cells more responsive to treatment, while also suppressing their growth and survival. We provide an in-depth analysis of scientific literature that investigates the manner in which inhibiting GSK-3β with various compounds might be used to treat, impede, and improve the therapeutic response in LC cells. Next, we suggested that GSK-3β inhibition might be a therapeutic option to increase patient survival in patients with LC. For this reason, further studies on this subject will be required in the coming years.</p> Graphical abstract <p></p>

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Harnessing GSK-3β inhibition for lung cancer therapy: emerging opportunities and challenges

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月11日

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  • Emad H. M. Hassanein,
  • Hanan S. Althagafy,
  • Hanan H. Abd- ElHafeez,
  • Islam M. Ibrahim,
  • Badrah S. Alghamdi

摘要

Lung cancer (LC) primarily affects men and is the third most common cause of cancer-related death worldwide. Treatment for LC involves many phases, each with specific challenges arising from the characteristics of malignancy and the limitations of chemotherapy. GSK-3β, a serine/threonine kinase factor, is essential for several signals that control important cellular functions and a variety of diseases, including cancer. GSK-3β regulates transcription factors through phosphorylation, which in turn activates signaling pathways such as PI3K/AKT/mTOR, Wnt/β-catenin, and NF-κB. These signaling pathways might affect LC. Additionally, targeting GSK-3β offers a promising approach to overcoming drug resistance in cancer therapy. Inhibiting GSK-3β has been demonstrated to boost chemotherapy sensitivity, making cancer cells more responsive to treatment, while also suppressing their growth and survival. We provide an in-depth analysis of scientific literature that investigates the manner in which inhibiting GSK-3β with various compounds might be used to treat, impede, and improve the therapeutic response in LC cells. Next, we suggested that GSK-3β inhibition might be a therapeutic option to increase patient survival in patients with LC. For this reason, further studies on this subject will be required in the coming years.

Graphical abstract