Gliomas and
melanomas are associated with dismal prognosis because of their marked intrinsic resistance to proapoptotic stimuli, such as conventional
chemotherapy and
radiotherapy, as well as their ability to escape immune cell attacks. In addition,
gliomas and
melanomas display pronounced neoangiogenesis.
Galectin-1 is a
hypoxia-sensitive
protein, which is abundantly secreted by
glioma and
melanoma cells, which displays marked proangiogenic effects. It also provides immune tolerogenic environments to
melanoma and
glioma cells through the killing of activated T cells that attack these
tumor cells.
Galectin-1 protects
glioma and
melanoma cells against cytotoxic insults (including
chemotherapy and
radiotherapy) through a direct role in the unfolded protein response. Altogether, these facts clearly point to
galectin-1 as an important target to be combated in
gliomas and
melanomas in order to: (1) weaken the defenses of these two types of
cancers against
radiotherapy,
chemotherapy and
immunotherapy/vaccine therapy; and (2) reinforce antiangiogenic
therapies. In the present article, we review the biochemical and molecular biology-related pathways controlled by
galectin-1, which are actually beneficial for
melanoma and
glioma cells, and therefore detrimental for
melanoma and
glioma patients.