| 研究実績の概要 |
In this fiscal year, we focused on investigating the role of EPS8L3 in hepatocellular carcinoma (HCC) using the JHH5 cell line. To achieve this, we performed knockdown of EPS8L3 expression using siRNA. The knockdown of EPS8L3 resulted in a significant decrease in cancer cell growth, and a reduction in tumor sphere formation.
To gain further insights into the molecular mechanisms underlying EPS8L3's function, we examined the expression of downstream target genes regulated by the Yes-associated protein (YAP), a key effector of the Hippo signaling pathway. Interestingly, the knockdown of EPS8L3 led to a downregulation of YAP target genes, implying a functional link between EPS8L3 and YAP signaling in HCC.
To further investigate the interaction between EPS8L3 and YAP, we employed CRISPR/Cas9 gene editing technology to introduce targeted mutations in the SH3 domain of EPS8L3. This domain is known to mediate protein-protein interactions, and we hypothesized that disrupting it might affect the binding between EPS8L3 and YAP. Indeed, our results demonstrated that the introduced mutations successfully prevented the interaction between EPS8L3 and YAP, providing valuable insights into the molecular basis of their functional association.
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