Hemoxygenase-1 genetic variants effects on breast cancer progression.

SCHWEITZER, K.; ALONSO, E.G.; MASCARÓ, M.; FERNÁNDEZ CHÁVEZ, L.; COLÓ, G.P.; ALONSO, E.N.; FERRONATO, M.J.; FERMENTO, M.E.; CURINO, A.C.; FACCHINETTI, M.M.

Mar del Plata

Otro; LXVII Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2022

SAIC

Hemoxygenase-1 (HO-1) is a microsomal enzyme that catalyzes the degradation of the heme group, and its C-terminal truncated form can translocate to the nucleus and perform functions at the transcriptional level. Our laboratory has already shown that HO-1 has antitumoraleffects in breast cancer. We have additionally confirmed that the HO-1 truncated form is not enzymatically active. The aim of this work was to study the effect of genetic overexpression of HO-1 variants(full-length form (FL), full-length form without enzymatic activity (H25A) and nuclear truncated form (T-HO1)) on cellular processes related to cancer development, and also the molecular mechanismsthrough which HO-1 would modulate the cellular processes investigated. To accomplish this goal, we used T47D human breast cancer cell line that was stably transfected with plasmids overexpressing HO-1 variants. To analyse cell behaviour between variants, we performed viability assays and flow cytometry, and to quantify differential protein expression we used immunofluorescence and western blot. We observed significant differences in cell viability betweenwild-type T47D cells and T47D cells overexpressing HO-1 variants. We found that the wild-type form is more proliferative than the FL-, H25A- and T-HO1-overexpressing forms (p