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Background <p>Oral squamous cell carcinoma(OSCC)is the most common oral cancer, featuring aggressive growth and high metastatic potential. Autophagy, the main cellular degradation mechanism, is closely linked to the progression of this cancer, but its specific role and related molecular mechanisms remain unclear. This study aimed to clarify the function of PRKCQ (protein kinase Cθ) in oral squamous cell carcinoma and explore how it affects cancer progression by regulating autophagy.</p> Methods <p>Tissue microarray, animal experiments and cell assays were used to detect the effect of PRKCQ knockdown on the proliferation and metastasis of OSCC. Transcriptomic analysis of cancer tissues was combined with data from public databases to analyze the correlation between PRKCQ and autophagy, and their association with patient prognosis. Cell experiments verified the effect of PRKCQ knockdown on autophagic flux and related functions. Cell transcriptomic analysis screened downstream target genes and verified the mechanism.</p> Results <p>The tissue microarray (TMA) revealed that PRKCQ is highly expressed in OSCC tissues and is negatively correlated with survival rate. Animal and cell experiments demonstrated that PRKCQ knockdown (KD) inhibited the proliferation and metastasis of OSCC cells. Through transcriptome analysis of OSCC tissues combined with data from The Cancer Genome Atlas (TCGA) database and the Human Autophagy Database (HADb), we revealed a close association between PRKCQ and autophagy, which involved in OSCC progression. Subsequent functional experiments demonstrated that PRKCQ KD disrupts autophagic flux by impairing lysosomal function and blocking autophagosome‒lysosome fusion. Furthermore, we found that knockdown of PRKCQ significantly suppressed the expression of TRIM22 (tripartite motif containing 22) through transcriptome analysis of PRKCQ KD cells. The overexpression of TRIM22 restored lysosomal function and autophagosome‒lysosome fusion, thereby restoring the progression of OSCC cells impaired by PRKCQ knockdown.</p> Conclusion <p>The PRKCQ-TRIM22 autophagic regulatory axis plays a key role in oral squamous cell carcinoma progression. This study clarifies the molecular mechanism by which PRKCQ promotes cancer development via autophagy regulation, providing potential new targets for targeted therapy.</p>

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PRKCQ-TRIM22 axis promotes proliferation and metastasis of oral squamous cell carcinoma via autophagosome‒lysosome pathway activation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月28日

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  • Jinghong Liu,
  • Jianbo Zhang,
  • Qunxiang Chen,
  • Weijia Qing,
  • Yongchun Peng,
  • Zhijing He,
  • Xi Zhou,
  • Huifeng Pi,
  • Bo Li,
  • Qingyun Lin,
  • Junxin Liu,
  • Fan Zhang,
  • Sheng Zhang,
  • Tengfei Fan

摘要

Background

Oral squamous cell carcinoma(OSCC)is the most common oral cancer, featuring aggressive growth and high metastatic potential. Autophagy, the main cellular degradation mechanism, is closely linked to the progression of this cancer, but its specific role and related molecular mechanisms remain unclear. This study aimed to clarify the function of PRKCQ (protein kinase Cθ) in oral squamous cell carcinoma and explore how it affects cancer progression by regulating autophagy.

Methods

Tissue microarray, animal experiments and cell assays were used to detect the effect of PRKCQ knockdown on the proliferation and metastasis of OSCC. Transcriptomic analysis of cancer tissues was combined with data from public databases to analyze the correlation between PRKCQ and autophagy, and their association with patient prognosis. Cell experiments verified the effect of PRKCQ knockdown on autophagic flux and related functions. Cell transcriptomic analysis screened downstream target genes and verified the mechanism.

Results

The tissue microarray (TMA) revealed that PRKCQ is highly expressed in OSCC tissues and is negatively correlated with survival rate. Animal and cell experiments demonstrated that PRKCQ knockdown (KD) inhibited the proliferation and metastasis of OSCC cells. Through transcriptome analysis of OSCC tissues combined with data from The Cancer Genome Atlas (TCGA) database and the Human Autophagy Database (HADb), we revealed a close association between PRKCQ and autophagy, which involved in OSCC progression. Subsequent functional experiments demonstrated that PRKCQ KD disrupts autophagic flux by impairing lysosomal function and blocking autophagosome‒lysosome fusion. Furthermore, we found that knockdown of PRKCQ significantly suppressed the expression of TRIM22 (tripartite motif containing 22) through transcriptome analysis of PRKCQ KD cells. The overexpression of TRIM22 restored lysosomal function and autophagosome‒lysosome fusion, thereby restoring the progression of OSCC cells impaired by PRKCQ knockdown.

Conclusion

The PRKCQ-TRIM22 autophagic regulatory axis plays a key role in oral squamous cell carcinoma progression. This study clarifies the molecular mechanism by which PRKCQ promotes cancer development via autophagy regulation, providing potential new targets for targeted therapy.