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Updated: Oct 10, 2025

Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics
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Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics

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Loss of TACC1 variant25 inducing cell proliferation and suppressing autophagy in head and neck squamous carcinoma

Pan Xu1,2,3,4,5, Ran Zhao1,2,3,4,5, Chen-Yang Zhang1

  • 1Department of Oral Mucosal Diseases, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Cell Death Discovery
|December 13, 2021
PubMed

Insights

Transforming acidic coiled-coil containing protein1 variant25 (TACC1v25) is downregulated in head and neck squamous cell carcinoma. TACC1v25 inhibits cancer progression by reducing proliferation and increasing autophagy via the ERK and AKT/mTOR pathways.

Area of Science:

  • Molecular oncology
  • Cellular biology
  • Cancer research

Background:

  • Transforming acidic coiled-coil containing protein1 (TACC1) plays roles in transcription, translation, and centrosome dynamics.
  • TACC1 dysregulation is linked to various cancers, with alternative splicing producing significant variants.
  • The specific roles of TACC1 variants in head and neck squamous cell carcinoma (HNSCC) are not well understood.

Purpose of the Study:

  • To investigate the expression patterns and biological functions of TACC1 variants in HNSCC.
  • To determine the specific role of TACC1 variant25 (TACC1v25) in HNSCC progression.
  • To elucidate the molecular mechanisms underlying TACC1v25's effects in HNSCC.

Main Methods:

  • Analysis of TACC1 variant expression in HNSCC tissues and cell lines.
  • Overexpression of TACC1v25 in HNSCC cell lines (Cal27 and Fadu).
  • Assessment of cell proliferation, autophagy markers (Beclin-1, LC3II/LC3I ratio), and signaling pathways (pERK, p-mTOR, AKT).

Main Results:

  • TACC1 variants show a distinct expression pattern in HNSCC.
  • TACC1v25 is significantly downregulated in HNSCC tissues and cell lines.
  • Overexpression of TACC1v25 suppressed proliferation and enhanced autophagy in HNSCC cells.
  • TACC1v25 overexpression led to decreased nuclear pERK and p-mTOR, and increased Beclin-1 and LC3II/LC3I ratio.
  • Autophagy was rescued by activating the AKT pathway with SC79.

Conclusions:

  • TACC1v25 inhibits HNSCC progression by reducing proliferation and promoting autophagy.
  • The tumor-suppressive effects of TACC1v25 are mediated through the ERK and AKT/mTOR signaling pathways.
  • TACC1v25 demonstrates potential as a therapeutic target or tumor suppressor in HNSCC.

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