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CKIP-1 silencing suppresses OSCC via mitochondrial homeostasis-associated TFAM/cGAS-STING signalling axis

Ji-Rong Xie1, Xiao-Jie Chen1,2, Gang Zhou1,2

  • 1State Key Laboratory of Oral and Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School and Hospital of Stomatology, Wuhan University, Wuhan, China.

Journal of Cellular and Molecular Medicine
|August 22, 2024
PubMed

Insights

Silencing casein kinase 2 interacting protein 1 (CKIP-1) suppresses oral squamous cell carcinoma (OSCC) growth. This occurs via the mitochondrial transcription factor A (TFAM)/cGAS-STING pathway, offering a potential therapeutic target for OSCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Oral squamous cell carcinoma (OSCC) lacks effective treatment targets.
  • Casein kinase 2 interacting protein 1 (CKIP-1) is a scaffold protein implicated in various diseases, but its role in OSCC is unknown.

Purpose of the Study:

  • To investigate the regulatory role of CKIP-1 in OSCC.
  • To elucidate the underlying molecular mechanisms of CKIP-1's action in OSCC.

Main Methods:

  • Analysis of CKIP-1 expression in OSCC tissues and cell lines.
  • Gain- and loss-of-function experiments to assess CKIP-1's impact on OSCC cell behavior.
  • Investigation of mitochondrial homeostasis markers, including mitochondrial transcription factor A (TFAM), reactive oxygen species (ROS), mitochondrial membrane potential, and the cGAS-STING pathway.
  • Utilized tetramethylpyrazine (TMP) to inhibit TFAM degradation and confirm pathway involvement.

Main Results:

  • CKIP-1 expression is elevated in OSCC tissues and cell lines.
  • CKIP-1 silencing suppressed OSCC cell malignant behaviors, enhanced apoptosis, and inhibited tumor growth.
  • Silencing CKIP-1 led to TFAM downregulation, increased ROS production, decreased mitochondrial membrane potential, and activated the cGAS-STING pathway.
  • The TFAM/cGAS-STING axis was confirmed to be involved in CKIP-1-silenced OSCC cells.

Conclusions:

  • CKIP-1 plays a significant role in promoting OSCC progression.
  • CKIP-1 silencing antagonizes OSCC via the TFAM/cGAS-STING axis, impacting mitochondrial homeostasis.
  • CKIP-1 represents a potential therapeutic target for oral squamous cell carcinoma treatment.
Keywords:
gene therapymitochondriaoral squamous cell carcinomasignal transduction

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