Browsing by Subject "OSCC"

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    Expression of p53 family members and CD44 in oral squamous cell carcinoma (OSCC) in relation to tumorigenesis
    (Murcia : F. Hernández, 2010) Bidaud, Pauline; Chasle, Jacques; Sichel, François; Rousseau, Stéphane; Petit, Pascal; Pottier, Didier; Picquenot, Jean Michel; Louis, Marie-Yolande; Lechevrel, Mathilde
    Oral squamous cell carcinomas (OSCCs) aredescribed as the result of a multistep tumorigenesisprocess. In order to develop useful diagnosis of pre-malignant lesions, expression of p53 family membersand the cancer stem cell (CSCs) marker, CD44v6, werestudied in histologically normal oral epithelium,precancerous lesions and succeeding invasive OSCCs.p53 was expressed focally in normal epithelium adjacentto tumors, while expression was high in intra-epithelialneoplasia and moderate in OSCC. p63 nuclear stainingwas important in basal and suprabasal layers ofhistologically normal oral mucosa and in immaturecompartments of premalignant lesions and cancer. Inepithelium without neoplasia, intense p73 staining wasobserved in the basal layer, while focal expression waspresent in suprabasal layers. Most immature dysplasticareas showed either high or moderate staining, whereasthose in OSCCs expressed low and moderate p73 levelexpression. CD44v6 was only expressed in poorlydifferentiated areas of epithelium, altered or not. p53,p63 and p73 positive stainings were statistically relatedin intra-epithelial neoplasia to tumours. Analysis ofTP53 mutations in 17% of tumours principally revealedG>A and A>G transitions. No relation was observedbetween this mutational profile and differentimmunostainings. In conclusion, our results support thatimmunostaining of p53 family members might behelpful in diagnosis and monitoring of high-risk pre-malignant lesions of oral epithelium. The combination ofstaining patterns of p63, p73αand CD44v6 enabled us to isolate phenotypic undifferentiated or transientamplifying areas, reflecting the immaturity of the tumourcell lineage. While CD44v6 expression is an interestingmarker of such epithelial cells, it is not specific enoughto be useful alone and other phenotypic markers areneeded.
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    Prognostic significance of E-cadherin, β-catenin and cyclin D1 in oral squamous cell carcinoma: a tissue microarray study
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Al-Rawi, Natheer; Al Ani, Muwaffaq; Quadri, Asif; Hamdoon, Zaid; Awwad, Aktham; Al Kawas, Sausan; Al Nuaim, Ahmed
    Objective. To study the prognostic significance of E-cadherin, β-catenin, and cyclin D1 expression in oral squamous cell carcinoma. Subjects and Methods. The study included 65 subjects with histologically confirmed squamous cell carcinoma. TMA blocks were prepared for immunohistochemical quantification of the expression of the three markers using IHC profiler and Immune ratio plugin of Image J. Results. E-cadherin expression was significantly correlated with histological grades and the metastasis status (p<0.05), whereas β-catenin expression was significantly correlated with smoking and tumor recurrence (P<0.05). Cyclin D1 expression was significantly correlated with depth of invasion and tumor recurrence. (p<0.05). Advanced tumor stage and depth of tumor invasion increases the risk of recurrence or death by 2.5 times (OR=2.53 and 0.84 respectively). Conclusion. High expression of β-catenin and cyclin D1 are significantly correlated with tumor recurrence and old age. Depth of invasion, low histological grade and old age were a significant predictor for the risk of having tumor recurrence and cancer related death.
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    Silencing of SETD6 inhibits the tumorigenesis of oral squamous cell carcinoma by inhibiting methylation of PAK4 and RelA
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Huang, Wentao; Liu, Hongjing; Lv, Tianzhu
    . Background. Oral squamous cell carcinoma (OSCC) is one of the most comment types of oral malignancies. SET-domain-containing protein 6 (SETD6) was recently identified as an important regulator of multiple signaling pathways through methylating protein substrates. Meanwhile, SETD6 is known to participate in multiple cancers. However, the role of SETD6 in OSCC remains unclear. Methods. Gene and protein expressions in OSCC cells or tissues were detected by RT-qPCR and western blot, respectively. In addition, CCK-8 assay was used to test the cell viability. A transwell assay was performed to measure cell migration and invasion. Flow cytometry was used to test cell apoptosis and cycle. Meanwhile, methylation-specific PCR (MSP) was used to detect the status of promoter methylation. Results. SETD6 was significantly upregulated in OSCC tissues. In addition, knockdown of SETD6 notably inhibited the proliferation and induced the apoptosis of OSCC cells. Furthermore, silencing of SETD6 notably suppressed the migration and invasion of OSCC cells. Meanwhile, SETD6 siRNA significantly inhibited the promoter methylation of RelA (NF-κB p65) and PAK4. Furthermore, SETD6 siRNA induced G1 arrest in OSCC cells. Conclusion. Knockdown of SETD6 inhibits the tumorigenesis of OSCC by suppressing promoter methylation of PAK4 and RelA. Therefore, our study might shed new light on exploring strategies for the treatment of OSCC.