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.

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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