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Updated: Jun 11, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
BANF1 knockdown impedes thyroid cancer development and boosts CD8+ T cell activity through PI3K/AKT/mTOR pathway
Chuanbing Liu1, Zhen Jia1, Dan Wei1
1Department of Endocrinology and Metabolism, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital, Shandong Institute of Nephrology Jinan, Shandong, China.
None:
Barrier to Autointegration Factor 1 (BANF1) is a highly evolutionarily conserved small DNA-binding protein, and its dysregulation has been implicated in the development of various diseases. This study seeks to elucidate the role of BANF1 in thyroid cancer and its relevance to tumor immunity. BANF1 expression levels were assessed using Western blot and RT-qPCR. The effects of BANF1 on thyroid cancer cell progression were evaluated using colony formation assays, EdU, Transwell migration/invasion assays, and Flow cytometry (FCM). The effects of BANF1 knockdown on CD8+ T cell viability and cytokine secretion were examined using CCK-8 and FCM assays. Furthermore, the influence of BANF1 on proteins associated with the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway was detected. Our results showed that BANF1 expression was significantly higher in thyroid cancer tissues compared with the adjacent tissues. BANF1 inhibition induced apoptosis and suppressed the proliferative, migratory, and invasive potential of thyroid cancer cells. However, BANF1 knockdown had no significant effect on the growth of transplanted tumors in BALB/c immunodeficient nude mice Moreover, inhibition of BANF1 enhanced CD8+ T cell proliferation and cytokine production. Mechanistically, BANF1 knockdown promoted activation of the PI3K/AKT/mTOR pathway. In summary, BANF1 knockdown suppresses thyroid cancer cell progression and enhances CD8+ T cell vitality, potentially through modulating the PI3K/AKT/mTOR signaling pathway in CD8+ T cells.
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