Abstract
Many cancers are initiated by the activation of oncogenes, which cause cancer phenotypes through a variety of disruptive mechanisms. FYN is a human proto-oncogene implicated in many cancers, especially those of the central nervous system and ovary. FYN encodes a non-receptor tyrosine kinase from the Src tyrosine kinase family, and has been shown to promote proliferation and metastasis. Our previous publication demonstrated that introduction of human FYN in the Drosophila eye resulted in a deleterious effect on eye structure, suggesting potential conserved functions across species. This study utilized the Gal4-UAS system to express a wildtype version of human FYN and a constitutively active form of its Drosophila ortholog, Src64B, in the eye and ovary of Drosophila melanogaster, to further explore their conserved functions. Our findings suggested that overexpression of FYN and Src64B in Drosophila eye tissue exhibited conserved developmental defects and a rough eye phenotype. FYN overexpression in the Drosophila ovary demonstrated accumulation of anterior egg chamber squamous cells without associated proliferative activity. These accumulated squamous cells exhibited altered expressions of apical, basolateral, and Par-complex polarity factors. Constitutive expression of Src64B showed similar phenotypes. These results indicate that the conserved oncogenic potential of FYN may be linked to changes in cell polarity signaling, which is considered a hallmark of cancer.
