Fig. 1
From: TRIM8: a double-edged sword in glioblastoma with the power to heal or hurt
Schematic representation of the TRIM8-PIAS3-STAT3 pathway, which leads to therapeutic resistance in GSCs. TRIM8 induces ubiquitin-mediated proteasomal degradation of PIAS3 and SOCS1, contributing to activation of STAT3 and subsequent promotion of expression of GSC-related markers and transcription factors, including MYC, SOX2, PROM1/CD133, POU2F1/OCT1, NANOG, MKI67, and NES. These markers and transcription factors play a functional role in stem cell acquisition, inhibition of differentiation, and enhancement of stem cell activity in this tumor type. In addition, STAT3 increases TRIM8 expression, leading to a positive TRIM8-STAT3 feedback loop in GBM. This offers new insight into how targeting TRIM8 or STAT3 could effectively affect GBM self-renewal and tumor growth