Simultaneous E-cadherin and PLEKHA7 expression negatively affects E-cadherin/EGFR mediated ovarian cancer cell growth.
Katia ReaFrancesca RoggianiLoris De CeccoFrancesco RaspagliesiMaria Luisa CarcangiuJoyce Nair-MenonMarina BagnoliIleana BortolomaiDelia MezzanzanicaSilvana CanevariAntonis KourtidisPanos Z AnastasiadisAntonella TomassettiPublished in: Journal of experimental & clinical cancer research : CR (2018)
These data represent a significant step towards untangling the role of E-cadherin in EOCs by assessing its positive effects on EGFR/CDK5 signaling and its contribution to cell growth. Hence, the inhibition of this signaling using a CDK5 inhibitor exerts a synergistic effect with cisplatin prompting on the design of new therapeutic strategies to inhibit growth of EOC cells. We assessed for the first time in EOC cells that PLEKHA7 induces changes in the asset of E-cadherin-containing cell-cell contacts thus inhibiting E-cadherin/EGFR crosstalk and leading to a less aggressive tumor phenotype. Accordingly, PLEKHA7 levels are lower in high grade EOC patient tumors and EOC patients with better outcomes display higher PLEKHA7 levels.
Keyphrases
- small cell lung cancer
- induced apoptosis
- epidermal growth factor receptor
- high grade
- tyrosine kinase
- cell cycle arrest
- single cell
- cell therapy
- cell cycle
- signaling pathway
- poor prognosis
- type diabetes
- oxidative stress
- case report
- electronic health record
- stem cells
- machine learning
- mesenchymal stem cells
- bone marrow
- weight loss