@article {RAMOS439, author = {DAVID RAMOS and ANA PELL{\'I}N-CARCEL{\'E}N and JAIME AGUST{\'I} and AMELIA MURGUI and ESPERANZA JORD{\'A} and ANTONIO PELL{\'I}N and CARLOS MONTEAGUDO}, title = {Deregulation of Glyceraldehyde-3-Phosphate Dehydrogenase Expression During Tumor Progression of Human Cutaneous Melanoma}, volume = {35}, number = {1}, pages = {439--444}, year = {2015}, publisher = {International Institute of Anticancer Research}, abstract = {Background/Aim: Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a highly abundant housekeeping gene. GAPDH overexpression has been reported in diverse types of human cancers including cutaneous melanoma. Our goal was to quantify GAPDH mRNA and protein expression in the whole spectrum of primary and metastatic melanomas in the search for a specific role for this ubiquitous molecule during tumor progression. Materials and Methods: Intratumoral GAPDH mRNA expression was quantified by real-time PCR in 71 cases, including 29 primary melanomas and 42 metastatic cases. Relative expression levels in thin (<=1 mm) and thick (\>1 mm) primary tumors and {\textquoteleft}in-transit{\textquoteright}, lymph node and distant metastases were compared. Similarly, protein expression was investigated by means of immunohistochemistry. Specific exons of GAPDH were analyzed by DNA sequencing. Results: GAPDH mRNA expression was significantly up-regulated in thick melanomas when compared to primary thin melanomas. Similar differences were also encountered between metastatic melanomas when compared to lymph-node metastatic melanomas. Interestingly, GAPDH protein immunoexpression was higher in thick melanomas and distant metastases than in thin tumors and lymph node metastases, respectively. However, no specific point-mutations in GAPDH-specific exons were found in any patient. Conclusion: Deregulation of GAPDH during melanoma progression was demonstrated in our series by mRNA and protein expression studies.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/35/1/439}, eprint = {https://ar.iiarjournals.org/content/35/1/439.full.pdf}, journal = {Anticancer Research} }