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<p>Cancer-associated fibroblasts (CAFs) have been shown to play a crucial role in the progression of non-small cell lung cancer (NSCLC). Exosomes derived from CAFs have emerged as important mediators of intercellular communication in the tumor microenvironment, contributing to cancer progression. Therefore, it is essential to further investigate the mechanisms by which CAF-derived exosomes regulate NSCLC. CAFs promoted NSCLC cell proliferation, invasion, and migration, while also suppressing radiosensitivity. We observed an upregulation of FAM83F expression in both NSCLC cells and NSCLC cells treated with conditioned medium from CAFs. Notably, CAF-derived exosomes were found to transfer FAM83F to NSCLC cells, thereby enhancing the malignant properties of the cancer cells. In contrast, FAM83F-deficient CAF-derived exosomes exerted inhibitory effects on NSCLC cell proliferation, invasion, and migration, while also sensitizing the cells to radiotherapy. FAM83F was found to interact with KIF23 in NSCLC cells, and the overexpression of KIF23 attenuated the effects induced by FAM83F-deficient exosomes in NSCLC cells. Moreover, FAM83F-deficient CAF-derived exosomes were effective in inhibiting tumor formation <i>in vivo</i>. Our findings highlight the crucial role of CAF-derived exosomal FAM83F in promoting NSCLC progression and conferring resistance to radiotherapy. Targeting this signaling pathway may offer promising therapeutic strategies for combating NSCLC progression and improving patient outcomes.</p>

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Cancer-associated fibroblast-derived exosomal FAM83F regulates KIF23 expression to promote the malignant progression and reduce radiosensitivity in non-small cell lung cancer

  • 期刊论文

  • 发表日期：

    2025年1月25日

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  • Yi Li,
  • Mingming Zhou,
  • Xiaogang Hu,
  • Tingting Xie,
  • Wenli Peng,
  • Lina Zhang,
  • Minxin Tang,
  • Rui Hu,
  • Yongpeng He

摘要

Cancer-associated fibroblasts (CAFs) have been shown to play a crucial role in the progression of non-small cell lung cancer (NSCLC). Exosomes derived from CAFs have emerged as important mediators of intercellular communication in the tumor microenvironment, contributing to cancer progression. Therefore, it is essential to further investigate the mechanisms by which CAF-derived exosomes regulate NSCLC. CAFs promoted NSCLC cell proliferation, invasion, and migration, while also suppressing radiosensitivity. We observed an upregulation of FAM83F expression in both NSCLC cells and NSCLC cells treated with conditioned medium from CAFs. Notably, CAF-derived exosomes were found to transfer FAM83F to NSCLC cells, thereby enhancing the malignant properties of the cancer cells. In contrast, FAM83F-deficient CAF-derived exosomes exerted inhibitory effects on NSCLC cell proliferation, invasion, and migration, while also sensitizing the cells to radiotherapy. FAM83F was found to interact with KIF23 in NSCLC cells, and the overexpression of KIF23 attenuated the effects induced by FAM83F-deficient exosomes in NSCLC cells. Moreover, FAM83F-deficient CAF-derived exosomes were effective in inhibiting tumor formation in vivo. Our findings highlight the crucial role of CAF-derived exosomal FAM83F in promoting NSCLC progression and conferring resistance to radiotherapy. Targeting this signaling pathway may offer promising therapeutic strategies for combating NSCLC progression and improving patient outcomes.