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<p>Traditional Chinese medicines have exhibited anticancer effects in tumors, which may provide novel therapeutic clues for cancer therapies. Non-small cell lung cancer (NSCLC) is the main subtype of lung cancer. This study discovers a novel regulatory mechanism influenced by berberine (BBR) in NSCLC, which is hoped to provide basic proof for its clinical transition. The results showed that BBR treatment inhibited cell proliferation, migration, and stemness and facilitated apoptosis of NSCLC cells in a dosage-dependent manner. BBR treatment inhibited the expression of FZD8, and NSCLC tissues and cells showed a high FZD8 expression. FZD8 overexpression reversed the inhibitory effects of BBR treatment on the malignant characteristics of NSCLC cells and the protein expression of Wnt3A and β-catenin. In addition, E2F1 transcriptionally activated FZD8 expression in NSCLC cells, and E2F1 silence hindered the malignant biological activities of NSCLC cells by regulating FZD8 expression. Moreover, E2F1 overexpression rescued the effects induced by BBR treatment on the key malignant phenotypes of NSCLC cells. Further, BBR treatment curbed tumor growth via regulating FZD8 expression. Collectively, BBR hampered the malignant progression of NSCLC by hindering the E2F1/FZD8 axis, which might provide experimental evidence for its clinical application.</p>

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Berberine hinders the malignant progression of non-small cell lung cancer via regulating E2F1/FZD8 signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月9日

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  • Shenping Liu,
  • Chunmei Tang

摘要

Traditional Chinese medicines have exhibited anticancer effects in tumors, which may provide novel therapeutic clues for cancer therapies. Non-small cell lung cancer (NSCLC) is the main subtype of lung cancer. This study discovers a novel regulatory mechanism influenced by berberine (BBR) in NSCLC, which is hoped to provide basic proof for its clinical transition. The results showed that BBR treatment inhibited cell proliferation, migration, and stemness and facilitated apoptosis of NSCLC cells in a dosage-dependent manner. BBR treatment inhibited the expression of FZD8, and NSCLC tissues and cells showed a high FZD8 expression. FZD8 overexpression reversed the inhibitory effects of BBR treatment on the malignant characteristics of NSCLC cells and the protein expression of Wnt3A and β-catenin. In addition, E2F1 transcriptionally activated FZD8 expression in NSCLC cells, and E2F1 silence hindered the malignant biological activities of NSCLC cells by regulating FZD8 expression. Moreover, E2F1 overexpression rescued the effects induced by BBR treatment on the key malignant phenotypes of NSCLC cells. Further, BBR treatment curbed tumor growth via regulating FZD8 expression. Collectively, BBR hampered the malignant progression of NSCLC by hindering the E2F1/FZD8 axis, which might provide experimental evidence for its clinical application.