Cdh1 stabilizes STING to boost innate immune activation in renal cell carcinoma, study finds
By
Pengda Liu
Summary
This article presents research by Zhu et al. on the role of the APC/C adaptor protein Cdh1 in stabilizing STING (a key innate immune sensor) to enhance antitumor immunity in clear cell renal cell carcinoma (ccRCC). While Cdh1 has traditionally been viewed as a tumor suppressor due to its role in mitotic integrity and cell cycle regulation, the study reveals a dual role: high Cdh1 mRNA expression correlates with poor prognosis in ccRCC but also with increased STING protein abundance. Mechanistically, Cdh1 binds to STING and protects it from ubiquitin-mediated degradation, thereby potentiating innate immune activation. This identifies a therapeutically exploitable link between Cdh1 abundance and antitumor immunity in kidney cancer.
Source
Twitter / XCdh1 stabilizes STING to boost innate immune activation in renal cell carcinoma, study findsscim.agKey quotes
· 5 pulledThe protein Cdh1 (Cdc20 homolog 1, also called Fizzy-related, encoded by FZR1) has tumor-suppressive activity because of its role in supporting mitotic integrity.
Zhu et al. identified a therapeutically exploitable link between high Cdh1 abundance and antitumor immunity in kidney cancer.
The authors found that Cdh1 bound to STING and protected it from ubiquitin-mediated degradation.
Although increased expression of mRNA encoding Cdh1 correlated with poor prognosis in clear cell renal cell carcinomas (ccRCCs), it also correlated with high abundance of the innate immune sensor STING.
The E3 ubiquitin ligase APC/C with its coactivator Cdh1 is generally considered to be a tumor suppressor, regulating genome stability and the G1/S transition of the cell cycle.
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