HPV disrupt the cytoskeleton in oral squamous cell carcinomas from non-oropharyngeal sites via the E-cadherin/Mena/SMA pathway

Bereczki-Temistocle, Despina Luciana; Jung, Ioan; Gurzu, Simona; Kovács, Zsolt; Chiciudean, Rebeca; Ormenișan, Alina; Banias, Laura

doi:10.1016/j.prp.2023.154723

Cited by 5 publications

(1 citation statement)

References 19 publications

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“…In the studies of OSCC, the high expression of ENAH in OSCC was associated with epithelial‐to‐mesenchymal transition (EMT) induced tumor progression and metastasis, as well as poor prognosis in OSCC patients. 15 , 16 The function and mechanism of ENAH‐202 in oral cancer are still unknown.…”

Section: Introductionmentioning

confidence: 99%

ENAH‐202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis

Zhang,

Chen,

Sun

et al. 2023

Cancer Medicine

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BackgroundWe aimed to demonstrate the regulatory effect of long non‐coding RNA (lncRNA) ENAH‐202 on oral squamous cell carcinoma (OSCC) development as well as its molecular mechanism.MethodsWe detected ENAH‐202 expression in OSCC tissues and cell lines by quantitative real‐time PCR (qPCR). The biological function of ENAH‐202 was assessed in vitro and in vivo using CCK‐8, colony formation assays, transwell assays, xenograft formation, and tail vein injection. The further molecular mechanism by which ENAH‐202 promoted OSCC progression was identified using RNA pull‐down, LS‐MS/MS analysis, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) assays.ResultsENAH‐202 was significantly upregulated in OSCC tissues and cells. ENAH‐202 promoted OSCC cell proliferation, migration, and invasion in vitro and in vivo. The expression of enabled homolog (ENAH) and epithelial‐to‐mesenchymal transition (EMT)‐related proteins was changed with the expression of ENAH‐202. Moreover, ENAH‐202 promoted the transcription of Vimentin (VIM) by binding with ZNF502, which can help ENAH‐202 promote OSCC progression.ConclusionsENAH‐202 facilitated OSCC cell proliferation and metastasis by regulating ZNF502/VIM axis, which played an important role in OSCC progression.

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Section: Introductionmentioning

confidence: 99%

ENAH‐202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis

Zhang,

Chen,

Sun

et al. 2023

Cancer Medicine

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Malignant Transformation of Normal Oral Tissue to Dysplasia and Early Oral Squamous Cell Carcinoma: An In Silico Transcriptomics Approach

Jamshidi,

Tavangar,

Shojaei

et al. 2024

Analytical Cellular Pathology

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Background: Oral squamous cell carcinoma (OSCC) is a prevalent and aggressive form of head and neck cancer, often diagnosed at advanced stages. Elucidating the molecular mechanisms involved in the malignant transformation from normal oral tissue to oral preinvasive lesions (OPL) and primary OSCC could facilitate early diagnosis and improve therapeutic strategies.Methods: Differentially expressed genes (DEGs) were identified from the GSE30784 dataset by comparing normal oral tissue, oral dysplasia, and primary OSCC samples. Cross‐validation was performed using an independent RNA‐seq dataset, GSE186775. Protein–protein interaction (PPI) network analysis, gene ontology annotation, and pathway enrichment analysis were conducted on the common DEGs. Hub genes were identified, and their prognostic significance was evaluated using survival analysis. Transcription factor (TF) enrichment analysis, cross‐validation, and immunohistochemistry analyses were also performed.Results: A total of 226 proteins and 677 interactions were identified in the PPI network, with 34 hub genes, including FN1, SERPINE1, PLAUR, THBS1, and ITGA6. Pathways such as “Formation of the cornified envelope,” “Keratinization,” and “Developmental biology” were enriched. Overexpression of SERPINE1, PLAUR, THBS1, and ITGA6 correlated with poor prognosis, while upregulation of CALML5 and SPINK5 was associated with favorable outcomes. NFIB emerged as the most significant TF‐regulating hub genes. Immunohistochemistry validated ITGA6 overexpression in primary OSCC. Cross‐validation using the RNA‐seq dataset supported the involvement of critical genes in the malignant transformation process.Conclusion: This study identified vital genes, pathways, and prognostic markers involved in the malignant transformation from normal oral tissue to OPL and primary OSCC, providing insights for early diagnosis and targeted therapy development. Cross‐validation with an independent RNA‐seq dataset and immunohistochemistry reinforced the findings, supporting the robustness of the identified molecular signatures.

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Correlation between human papillomavirus protein expression and clinicopathological features in oral squamous cell carcinoma

Wang,

Jiang,

Lee Chen

2024

Int J Immunopathol Pharmacol

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Objective Given the implications of concurrent human papilloma viral infection (HPV) in the prognostic course and implications on therapeutic approached of patients with oral squamous cell carcinoma (OSCC), we seek to investigate the implications that P16 expression has on the clinical course and pathological appearance of patients with OSCC and concurrent infection. Methods Using S-P immunohistochemistry, we examined the expression of P16 and Ki67 in 460 patients with OSCC. We compared the expression of the protein between the tumor cells and normal epithelial mucosa within the same patient. The clinical and pathological characteristics (including gender, age, histological grade, lymph node metastasis, clinical stage, clinical recurrence, tumor diameter, Ki67 proliferation index) were analyzed by stratification statistically. Results In total 460 cases of OSCC were identified and expression of P16 was significantly higher in the OSCC group compared to the normal mucosal epithelial group (X2 = 60.545, p = .000). There also appear to be a gender predilection as the expression was higher in females compared to males (0.218 vs. 0.144, X2 = 3.921, p = .048). Younger age also appears to be a predictive factor as those under 35 years old had higher expression of the protein compared to those over 35 years old (0.294 vs. 0.157, X2 = 4.230, p = .040). P16 positivity showed a significant positive correlation with histologic grade (X2 = 4.114, p = .043). In addition, the positive rate of P16 was higher in patients with ki67 over 85% (0.455 vs. 0.160, X2 = 6.667, p = .023). Conclusion OSCC with HPV infection tends to occur more frequently in female patients and those under 35 years of age. HPV infection with expression of the P16 and ki67 protein may promote the proliferation and growth of OSCC at a higher frequency.

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HPV disrupt the cytoskeleton in oral squamous cell carcinomas from non-oropharyngeal sites via the E-cadherin/Mena/SMA pathway

Cited by 5 publications

References 19 publications

ENAH‐202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis

ENAH‐202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis

Malignant Transformation of Normal Oral Tissue to Dysplasia and Early Oral Squamous Cell Carcinoma: An In Silico Transcriptomics Approach

Correlation between human papillomavirus protein expression and clinicopathological features in oral squamous cell carcinoma

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