Lesser-Known Molecules in Ovarian Carcinogenesis

Abstract

Currently, the deciphering of the signaling pathways brings about new advances in the understanding of the pathogenic mechanism of ovarian carcinogenesis, which is based on the interaction of several molecules with different biochemical structure that, consequently, intervene in cell metabolism, through their role as regulators in proliferation, differentiation, and cell death. Given that the ensemble of biomarkers in OC includes more than 50 molecules the interest of the researchers focuses on the possible validation of each one's potential as prognosis markers and/or therapeutic targets. Within this framework, this review presents three protein molecules: ALCAM, c-FLIP, and caveolin, motivated by the perspectives provided through the current limited knowledge on their role in ovarian carcinogenesis and on their potential as prognosis factors. Their structural stability, once altered, triggers the initiation of the sequences characteristic for ovarian carcinogenesis, through their role as modulators for several signaling pathways, contributing to the disruption of cellular junctions, disturbance of pro-/antiapoptotic equilibrium, and alteration of transmission of the signals specific for the molecular pathways. For each molecule, the text is built as follows: (i) general remarks, (ii) structural details, and (iii) particularities in expression, from different tumors to landmarks in ovarian carcinoma.

Figure 1

Graphical scheme that illustrates the general structures and action principles for ALCAM, c-FLIP, and caveolin (RTKs: tyrosine kinase receptors, OD: caveolin scaffolding domain, Fas-R/Fas-L, TRAIL/TRAIL-R (DR4, DR5), TNF/TNF-R: death-receptor mediated apoptosis pathway, DISC: Death Inducing Signaling Complex, cas-8: caspase-8, cas-10: caspase-10, and eNOS, Src, ErbB-2/MAPK, Erk, Wnt, NF-κB, and PI3K/AKT/mTOR: signaling pathways).