The Expression of the Ubiquitin Ligase SIAH2 (Seven In Absentia Homolog 2) Is Increased in Human Lung Cancer

• DOI: 10.1371/journal.pone.0143376
• Publication Date: 2015-11-18T18:45:23Z
• Authors: Paula Moreno; Maribel Lara-Chica; Rafael Soler-Torr...; Teresa Caro; Manuel Medina; Antonio Álvarez; Ángel Salvatierra; Eduardo Muñoz; Marco A. Calzado
• Keywords: Male; 0301 basic medicine; Lung Neoplasms; Science; Ubiquitin-Protein Ligases; Primary Cell Culture; Gene Expression; Adenocarcinoma of Lung; Adenocarcinoma; Protein Serine-Threonine Kinases; Cohort Studies; 03 medical and health sciences; Fluorodeoxyglucose F18; Humans; RNA, Messenger; Aged; Neoplasm Staging; Q; R; Nuclear Proteins; Biological Transport; Middle Aged; Protein-Tyrosine Kinases; 3. Good health; Carcinoma, Squamous Cell; Medicine; Female; Research Article

Lung cancer is the leading cause of cancer-related deaths worldwide. Overall 5-year survival has shown little improvement over last decades. Seven in absentia homolog (SIAH) proteins are E3 ubiquitin ligases that mediate proteasomal protein degradation by poly-ubiquitination. Even though SIAH play a key role several biological processes, their human remains controversial. The aim study was to document SIAH2 expression pattern at different levels (mRNA, level and immunohistochemistry) non-small cell lung (NSCLC) samples compared surrounding healthy tissue from same patient, analyse association with clinicopathological features.One hundred fifty-two patient cohort treated surgically for primary were obtained study. Genic analysed clinic-pathologic variables.The present first analyze (RNA, (NSCLC). We found significantly enhanced adenocarcinoma (ADC) squamous (SCC). Paradoxically, non-significant changes RNA found, suggesting post-traductional regulatory mechanism. More importantly, an increased correlation between tumor grade detected, this could be used as prognostic biomarker predict progression. Likewise, showed strong positive fluorodeoxyglucose (2-deoxy-2(18F)fluoro-D-glucose) uptake NSCLC, which may assist clinicians stratifying patients overall risk poor survival. Additionally, we described inverse one its substrates, serine/threonine kinase DYRK2.Our results provide insight into potential use novel target treatment.