| Summary: | <p>PRMT5 is a major type II arginine methyltransferase and plays a crucial role in
tumorigenesis. PRMT5 is overexpressed in multiple tumour cell lines, and a high level
of PRMT5 was identified as an independent factor for poor clinical outcomes in
patients with cancer. PRMT5 has been identified as a potential clinical target for
antitumour therapy to enable the treatment of cancers efficiently and selectively.
However, studies on the role of PRMT5 are limited and there is a need to understand
the mechanisms underlying the biological function of PRMT5 and its therapeutic
potential. In this study, we have uncovered a functional role for the PRMT5-E2F1 axis
on different aspects of cancer cell biology, including cancer cell viability, apoptosis,
migration, invasion, and adhesion. Additionally, we performed a genome-wide
expression analysis and identified a group of E2F1 targets that modulate cell adhesion
and cellular migratory pattern, resulting in metastasis and invasion, via a PRMT5-
dependent mechanism. Furthermore, the expression of PRMT5 and E2F1 was
correlated, with high levels of PRMT5 and E2F1 indicating poor clinical outcomes.
This study is the first time to show that the PRMT5-E2F1 axis influences cancer cell
growth and division, and also augments the migration and invasive properties of
tumour cells. As a positive regulator of the E2F1 axis, this strengthens the case for the
use of inhibitors for PRMT5 as a viable therapeutic target, and further suggests the
clinical utility of drugs targeting PRMT5.</p>
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