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<p>Lung cancer remains the leading cause of cancer-related deaths worldwide. While the Family with sequence similarity 72 member A (FAM72A) gene has been implicated in various cancers, its role in lung cancer is yet to be determined. This study aimed to investigate the role of FAM72A in lung cancer and the underlying mechanism. Bioinformatic analysis of The Cancer Genome Atlas-Lung Adenocarcinoma (TCGA-LUAD) dataset revealed that FAM72A was significantly upregulated in lung adenocarcinoma tissues, and high FAM72A expression was closely associated with poor patient prognosis. Western blot analysis revealed that FAM72A protein expression was significantly upregulated in multiple lung cancer cell lines (A549, H1299, and H460) compared to normal lung epithelial cells. Through a series of assays including flow cytometry, MTT, clone formation, wound healing, and Transwell experiments, we demonstrated that knockdown of FAM72A via shRNA effectively suppressed proliferation and migration in A549 and H1299 cells, while promoting apoptosis. Additionally, in vivo studies using a mouse xenograft model confirmed that FAM72A knockdown inhibited tumor growth. Mechanistic analyses showed that FAM72A knockdown is associated with inactivation of the NF‑κB signaling pathway, as knockdown led to decreased expression of p-IkBα, p-IKKα, p-NF-κB, Cyclin D1, and PCNA. In conclusion, our findings demonstrate that FAM72A contributes to lung cancer progression by regulating the activity of the NF‑κB signaling pathway, suggesting its potential as a therapeutic target for lung cancer.</p>

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FAM72A is associated with lung cancer proliferation and migration via the NF‑κB signaling pathway

  • 期刊论文

  • 发表日期：

    2026年5月23日

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  • Qinhua Gu,
  • Qibin Shen,
  • Tiancheng Liu,
  • Lili Jin,
  • Weiwei Min

摘要

Lung cancer remains the leading cause of cancer-related deaths worldwide. While the Family with sequence similarity 72 member A (FAM72A) gene has been implicated in various cancers, its role in lung cancer is yet to be determined. This study aimed to investigate the role of FAM72A in lung cancer and the underlying mechanism. Bioinformatic analysis of The Cancer Genome Atlas-Lung Adenocarcinoma (TCGA-LUAD) dataset revealed that FAM72A was significantly upregulated in lung adenocarcinoma tissues, and high FAM72A expression was closely associated with poor patient prognosis. Western blot analysis revealed that FAM72A protein expression was significantly upregulated in multiple lung cancer cell lines (A549, H1299, and H460) compared to normal lung epithelial cells. Through a series of assays including flow cytometry, MTT, clone formation, wound healing, and Transwell experiments, we demonstrated that knockdown of FAM72A via shRNA effectively suppressed proliferation and migration in A549 and H1299 cells, while promoting apoptosis. Additionally, in vivo studies using a mouse xenograft model confirmed that FAM72A knockdown inhibited tumor growth. Mechanistic analyses showed that FAM72A knockdown is associated with inactivation of the NF‑κB signaling pathway, as knockdown led to decreased expression of p-IkBα, p-IKKα, p-NF-κB, Cyclin D1, and PCNA. In conclusion, our findings demonstrate that FAM72A contributes to lung cancer progression by regulating the activity of the NF‑κB signaling pathway, suggesting its potential as a therapeutic target for lung cancer.