PERSONAL DE APOYO
GOMEZ Silvina Esther
artículos
Título:
SPINK7 expression changes accompanied by HER2, P53 and RB1 can be relevant in predicting oral squamous cell carcinoma at a molecular level
Autor/es:
PENNACCHIOTTI, GINA; VALDÉS-GUTIÉRREZ, FABIO; GONZÁLEZ-ARRIAGADA, WILFREDO ALEJANDRO; MONTES, HÉCTOR FEDERICO; PARRA, JUDITH MARIA ROXANA; GUIDA, VALERIA ANDREA; GÓMEZ, SILVINA ESTHER; GUERRERO-GIMENEZ, MARTIN EDUARDO; FERNANDEZ-MUÑOZ, JUAN MANUEL; ZOPPINO, FELIPE CARLOS MARTIN; CARÓN, RUBÉN WALTER; EZQUER, MARCELO EDUARDO; FERNÁNDEZ-RAMIRES, RICARDO; BRUNA, FLAVIA ALEJANDRA
Revista:
Scientific Reports
Editorial:
Nature Research
Referencias:
Año: 2021 vol. 11
Resumen:
The oral squamous cell carcinoma (OSCC), which has a high morbidity rate, affects patients worldwide. Changes in SPINK7 in precancerous lesions could promote oncogenesis. Our aim was to evaluate SPINK7 as a potential molecular biomarker which predicts OSCC stages, compared to: HER2, TP53, RB1, NFKB and CYP4B1. This study used oral biopsies from three patient groups: dysplasia (n = 33), less invasive (n = 28) and highly invasive OSCC (n = 18). The control group consisted of clinically suspicious cases later to be confirmed as normal mucosa (n = 20). Gene levels of SPINK7, P53, RB, NFKB and CYP4B1 were quantified by qPCR. SPINK7 levels were correlated with a cohort of 330 patients from the TCGA. Also, SPINK7, HER2, TP53, and RB1, were evaluated by immunohistofluorescence. One-way Kruskal?Wallis test and Dunn´s post-hoc with a p < 0.05 significance was used to analyze data. In OSCC, the SPINK7 expression had down regulated while P53, RB, NFKB and CYP4B1 had up regulated (p < 0.001). SPINK7 had also diminished in TCGA patients (p = 2.10e-6). In less invasive OSCC, SPINK7 and HER2 proteins had decreased while TP53 and RB1 had increased with respect to the other groups (p < 0.05). The changes of SPINK7 accompanied by HER2, P53 and RB1 can be used to classify the molecular stage of OSCC lesions allowing a diagnosis at molecular and histopathological levels.