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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.
Abstract:
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.
Insights
Barrier to Autointegration Factor 1 (BANF1) is elevated in thyroid cancer, suppressing tumor growth and enhancing CD8+ T cell immunity via the PI3K/AKT/mTOR pathway.
Area of Science:
- Molecular Biology
- Cancer Research
- Immunology
Background:
- Barrier to Autointegration Factor 1 (BANF1) is an evolutionarily conserved DNA-binding protein implicated in various diseases.
- Dysregulation of BANF1 is linked to disease development, prompting investigation into its role in specific cancers.
Purpose of the Study:
- To investigate the role of BANF1 in thyroid cancer progression.
- To determine the impact of BANF1 on tumor immunity, specifically CD8+ T cell responses.
- To elucidate the underlying molecular mechanisms, including the PI3K/AKT/mTOR pathway.
Main Methods:
- BANF1 expression analyzed by Western blot and RT-qPCR.
- Thyroid cancer cell progression assessed via colony formation, EdU, Transwell, and Flow Cytometry (FCM).
- CD8+ T cell viability and cytokine secretion evaluated using CCK-8 and FCM assays; PI3K/AKT/mTOR pathway proteins analyzed.
Main Results:
- BANF1 expression is significantly higher in thyroid cancer tissues than adjacent tissues.
- BANF1 inhibition induced apoptosis and suppressed cancer cell proliferation, migration, and invasion.
- BANF1 knockdown enhanced CD8+ T cell proliferation and cytokine production, activating the PI3K/AKT/mTOR pathway.
Conclusions:
- BANF1 knockdown suppresses thyroid cancer cell progression.
- BANF1 inhibition enhances CD8+ T cell vitality and function.
- Modulation of the PI3K/AKT/mTOR pathway is implicated in BANF1's effects on thyroid cancer and immunity.
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