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Lesser-Known Molecules in Ovarian Carcinogenesis.

Lozneanu L, Cojocaru E, Giuşcă SE, Cărăuleanu A, Căruntu ID - Biomed Res Int (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Morpho-Functional Sciences, University of Medicine and Pharmacy "Grigore T. Popa", 16 University Street, 700115 Iaşi, Romania.

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.

No MeSH data available.


Related in: MedlinePlus

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).
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Related In: Results  -  Collection


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fig1: 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).

Mentions: Thus, it is believed that the membranous expression of ALCAM reflects the maintenance of intercellular stability (Figure 1) and that the cytoplasmic location, resulting from rearrangement of the intercellular junctions, characterizes tumor cells with high potential for invasion and metastasis [23]. This cytoplasmic specificity discriminates the advanced stages from the early ones, which designates ALCAM as a useful marker in the attempt to prove the effect of destruction of the intercellular binding, in tumor versus normal context [23]. Consequently, the decrease or absence of ALCAM membrane expression indicates a poor outcome in OC and can be useful in the identification of patients at risk, who need a more frequent follow-up and alternative treatment [23].


Lesser-Known Molecules in Ovarian Carcinogenesis.

Lozneanu L, Cojocaru E, Giuşcă SE, Cărăuleanu A, Căruntu ID - Biomed Res Int (2015)

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).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4538335&req=5

fig1: 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).
Mentions: Thus, it is believed that the membranous expression of ALCAM reflects the maintenance of intercellular stability (Figure 1) and that the cytoplasmic location, resulting from rearrangement of the intercellular junctions, characterizes tumor cells with high potential for invasion and metastasis [23]. This cytoplasmic specificity discriminates the advanced stages from the early ones, which designates ALCAM as a useful marker in the attempt to prove the effect of destruction of the intercellular binding, in tumor versus normal context [23]. Consequently, the decrease or absence of ALCAM membrane expression indicates a poor outcome in OC and can be useful in the identification of patients at risk, who need a more frequent follow-up and alternative treatment [23].

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Morpho-Functional Sciences, University of Medicine and Pharmacy "Grigore T. Popa", 16 University Street, 700115 Iaşi, Romania.

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.

No MeSH data available.


Related in: MedlinePlus