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Updated: Dec 12, 2025

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Published on: July 8, 2021
Deregulation of desmosomal proteins and extracellular matrix proteases in odontogenic keratocyst
Marina Gonçalves Diniz1, Filipe Fideles Duarte-Andrade2, Fernanda Stussi3
1Department of Pathology, Biological Sciences Institute, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, Brazil.
Objective:
Odontogenic keratocyst (OKC) is a benign lesion that tends to recur after surgical treatment. In an attempt to clarify the molecular basis underlining the OKC pathobiology, we aimed to analyze its proteomic profile.
Materials And Methods:
We compared the proteomic profiles of five OKC and matched normal oral mucosa by using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Then, we performed enrichment analysis and a literature search for the immunoexpression of the proteomics targets.
Results:
We identified 1,150 proteins and 72 differently expressed proteins (log2 fold change ≥ 1.5; p < .05). Twenty-seven peptides were exclusively detected in the OKC samples. We found 35 enriched pathways related to cell differentiation and tissue architecture, including keratinocyte differentiation, keratinization, desmosome, and extracellular matrix (ECM) organization and degradation. The immunoexpression information of 11 out of 50 proteins identified in the enriched pathways was obtained. We found the downregulation of four desmosomal proteins (JUP, PKP1, PKP3, and PPL) and upregulation of ECM proteases (MMP-2, MMP-9, and cathepsins).
Conclusions:
Proteomic analysis strengthened the notion that OKC cells have a similar proteomic profile to oral keratinocytes. Contextual investigation of the differentially expressed proteins revealed the deregulation of desmosome proteins and ECM degradation as important alterations in OKC pathobiology.
Insights
Odontogenic keratocyst (OKC) proteomic analysis reveals altered desmosome proteins and extracellular matrix degradation, offering insights into its recurrence. This study compared OKC and normal oral tissue proteomes.
Area of Science:
- Oral pathology
- Proteomics
- Molecular biology
Background:
- Odontogenic keratocyst (OKC) is a benign odontogenic tumor known for its high recurrence rate after surgical treatment.
- Understanding the molecular mechanisms underlying OKC pathobiology is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To elucidate the molecular basis of Odontogenic Keratocyst (OKC) pathobiology by analyzing its proteomic profile.
- To compare the proteomic profiles of OKC and matched normal oral mucosa to identify differentially expressed proteins and pathways.
Main Methods:
- Proteomic analysis was performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS) on five OKC samples and matched normal oral mucosa.
- Enrichment analysis and literature search were conducted to investigate the immunoexpression of identified proteomics targets.
Main Results:
- A total of 1,150 proteins were identified, with 72 differentially expressed proteins (log2 fold change ≥ 1.5; p < .05).
- Thirty-five enriched pathways related to cell differentiation and tissue architecture were identified, including keratinocyte differentiation, keratinization, desmosome, and extracellular matrix (ECM) organization and degradation.
- Downregulation of desmosomal proteins (JUP, PKP1, PKP3, PPL) and upregulation of ECM proteases (MMP-2, MMP-9, cathepsins) were observed in OKC.
Conclusions:
- Proteomic analysis confirms that OKC cells share similarities with oral keratinocytes at the proteomic level.
- Deregulation of desmosome proteins and ECM degradation are significant alterations contributing to OKC pathobiology.
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