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TCOF1 Regulates Tumor Cell Migration Through p53-Dependent Mitochondrial Homeostasis and F-Actin Dynamics

Yuanyuan Jiang1, Yao Wei1, Daikang Yang1

  • 1Department of Cell Biology and Genetics, School of Pre-Clinical Medicine, Guangxi Medical University, Nanning 530021, China.

Current Issues in Molecular Biology
|May 27, 2026
PubMed

Insights

TCOF1 deficiency inhibits tumor cell migration by disrupting actin polymerization and mitochondrial function. This impacts cell motility and energy metabolism through a p53-dependent pathway, revealing TCOF1

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • TCOF1 deficiency is linked to cellular dysfunction, but its roles in mitochondrial homeostasis and cytoskeletal regulation are not fully understood.
  • Understanding TCOF1's function is crucial for elucidating mechanisms of cell motility and energy metabolism.
  • The precise molecular pathways involving TCOF1 in these processes require further investigation.

Purpose of the Study:

  • To investigate the role of TCOF1 in tumor cell migration and cytoskeletal regulation.
  • To explore the impact of TCOF1 deficiency on mitochondrial homeostasis and energy metabolism.
  • To elucidate the molecular mechanisms by which TCOF1 influences these cellular functions, particularly the p53-mitochondrial axis.

Main Methods:

  • Cell migration assays were performed to assess the effect of TCOF1 deficiency on tumor cell motility.
  • F-actin polymerization and cytoskeletal integrity were analyzed using microscopy and biochemical methods.
  • Mitochondrial function, including energy metabolism and biogenesis, was evaluated in TCOF1-deficient cells.
  • Western blotting was used to determine the protein levels of p53 and other relevant factors.

Main Results:

  • TCOF1 deficiency significantly inhibited tumor cell migration and impaired F-actin polymerization, affecting cell morphology and motility.
  • Cells lacking TCOF1 exhibited mitochondrial dysfunction, characterized by aberrant energy metabolism and reduced mitochondrial biogenesis.
  • TCOF1 deficiency led to decreased p53 protein levels, suggesting a role for TCOF1 in regulating mitochondrial homeostasis via a p53-dependent pathway.

Conclusions:

  • TCOF1 plays a critical role in maintaining cytoskeletal dynamics, specifically F-actin assembly, which is essential for cell migration.
  • TCOF1 is involved in regulating mitochondrial homeostasis and energy metabolism, potentially through a p53-dependent pathway.
  • Our findings reveal TCOF1's multifaceted role in cellular functions, impacting both cytoskeletal integrity and mitochondrial health, with implications for cancer research.
Keywords:
F-actinSTORMTCOF1mitochondrial dysfunctionp53

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