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<p>Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer, accounting for 80% of lung cancer types, with a high metastasis rate and mortality. Here, this experiment investigated the effects of MFAP4 in NSCLC and its molecular mechanisms of ferroptosis in NSCLC. Patients with NSCLC and normal volunteer were obtained from our hospital. The mRNA and protein expression levels of MFAP4 were upregulated in a mouse model of NSCLC. MFAP4 expression levels in cancer cells of NSCLC model through Single Cell Analysis. Sh-MFAP4 reduced cancer growth, and increased Mitochondrial oxidation-induced ferroptosis in mice model of cancer. MFAP4 promoted cell growth, and reduced Mitochondrial oxidation of NSCLC. Si-MFAP4 increased Mitochondrial oxidation of NSCLC. MFAP4 induced FAK expression of NSCLC through the inhibition of FAK Ubiquitination. The m6A/METTL3 modifies MFAP4 expression stability in model of NSCLC by YTHDF1. In conclusion, MFAP4 induced FAK expression to reduce Mitochondrial oxidation-induced ferroptosis of NSCLC model through the inhibition of FAK Ubiquitination. Targeting MFAP4 is thus a potentially effective therapeutic strategy for patients with NSCLC or other cancer.</p>

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MFAP4 promotes cell prognosis of non-small cell lung cancer through the inhibition of ferroptosis by FAK

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月8日

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  • Xiaofeng Li,
  • Chunwei Xu,
  • Yonghua Min,
  • Youcai Zhu,
  • Zhanqiang Zhai

摘要

Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer, accounting for 80% of lung cancer types, with a high metastasis rate and mortality. Here, this experiment investigated the effects of MFAP4 in NSCLC and its molecular mechanisms of ferroptosis in NSCLC. Patients with NSCLC and normal volunteer were obtained from our hospital. The mRNA and protein expression levels of MFAP4 were upregulated in a mouse model of NSCLC. MFAP4 expression levels in cancer cells of NSCLC model through Single Cell Analysis. Sh-MFAP4 reduced cancer growth, and increased Mitochondrial oxidation-induced ferroptosis in mice model of cancer. MFAP4 promoted cell growth, and reduced Mitochondrial oxidation of NSCLC. Si-MFAP4 increased Mitochondrial oxidation of NSCLC. MFAP4 induced FAK expression of NSCLC through the inhibition of FAK Ubiquitination. The m6A/METTL3 modifies MFAP4 expression stability in model of NSCLC by YTHDF1. In conclusion, MFAP4 induced FAK expression to reduce Mitochondrial oxidation-induced ferroptosis of NSCLC model through the inhibition of FAK Ubiquitination. Targeting MFAP4 is thus a potentially effective therapeutic strategy for patients with NSCLC or other cancer.