KO MAT2A to further inhibit hypomorphic PRMT5 in MATPdeficient TNBC cells for metastasis suppression in vitro and in vivo
DOI:
https://doi.org/10.61173/z80m6s32Keywords:
Methylthioadenosine (MTA), Methylthioadenosine phosphorylase (MATP), Methionine adenosyltransferase II alpha (MAT2A), Triplenegative breast cancer (TNBC), S-adenosylmethionine (SAM), eIF4E, FGFR3Abstract
Triple-negative breast cancer is one of the common types with the lack of three joint receptors, ER, PR, and HER2, which leads to inadequate responses for current breast cancer targeting therapy. Previous studies have reported that MTAP deletion confers enhanced sensitivity for PRMT5 inhibition, and inhibition of PRMT5 suppresses cell growth by decreasing arginine methylation of eIF4E and FGFR3. The KO of MAT2A will reduce the level of SAM, which is the substrate for arginine methylation, to inhibit PRMT5 and reduce cell proliferation. This study investigates the comparison of effects for MAT2A KO in MATP-deficient and MTAP+/+ TNBC cells in vivo and in vitro..
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