DDX17 (DEAD-Box Helicase 17)

Rescue experiments demonstrated that re-expression of Sh2b1-T1, but not Sh2b1-T2, reversed the impairment of osteoblast differentiation triggered by Ddx17 knockdown. Taken together, these findings underscore the critical role of the Prmt1-Ddx17-Sh2b1 axis in regulating osteoblast differentiation and suggest this axis as a promising therapeutic target for osteoporosis.

Functionally, DDX17 regulates RNA metabolism, DNA repair, and protein interactions. It is linked to chronic non-infectious diseases: promoting tumor progression via pathways like Wnt/β-catenin; protecting myocardial function in cardiovascular diseases; and involving in neurological disorders.This review provides insights for exploring its biological functions and clinical applications.

Clinically, high OLR1+ macrophage infiltration correlated with shorter survival across independent cohorts. These findings establish a hypoxia-ETS1-NS-macrophage axis as a key mechanism sustaining ccRCC progression and highlight actionable targets for disrupting protumorigenic immune niches through modulation of the NS pathway.

Previous studies have shown that Cfz is associated with a higher incidence of severe adverse cardiac effects than bortezomib (Btz); however, the underlying mechanisms remain to be elucidated. Therefore, the overexpression of SENP1 using AAV vectors alleviates Cfz-induced cardiotoxicity in mice. In summary, our findings reveal a previously unknown role of the SENP1-DDX17 axis in protecting against cardiotoxicity induced by Cfz, providing a potential foundation for developing therapeutic strategies to mitigate cardiac side effects in the clinical management of MM patients.

Upon DNA damage induced by camptothecin or actinomycin D (Act D), both targeting topoisomerase I, or by 1-methyl-3-nitro-1-nitrosoguanidine (MNNG), an alkylating agent that generates apurinic/apyrimidinic sites, A3B accumulates at the nucleolar rim and interior...Conversely, immunoprecipitation-mass spectrometry with data-independent acquisition (IP-MS DIA) revealed increased interactions between A3B and RNA helicases such as DDX17 and DDX21, which are known R-loop-binding proteins, following MNNG or Act D treatment. Our results demonstrate that A3B-induced secondary DNA damage occurs in the nucleolus after DNA damage, providing new insights into the acquisition of cancer diversity involving A3B and the DNA damage response in the nucleolus.

Our results suggest that CHIP exerts a tumor-suppressive phenotype in CRC by destruction of DDX17, thereby attenuating β-catenin-driven oncogenic processes. Altogether, this study identifies a novel "CHIP-DDX17-β-catenin" axis as a critical regulatory mechanism in CRC.

These findings suggest a role of DDX17 in promoting the progression of PCa by binding and blocking SPOP ubiquitination of AR. This study elucidated a novel mechanism through which the RNA helicase DDX17 can promote PCa progression through its interaction with SPOP, thereby enhancing AR stability by inhibiting AR ubiquitination.

METTL3-mediated m6A modification stabilizes DDX17 to suppress EC cell proliferation, migration, and invasion through an IGF2BP2-dependent mechanism by inactivating the PI3K/AKT pathway.

These findings indicated that DDX17 may be considered a potential prognostic biomarker and a promising target for novel immunotherapeutic approaches in cancer treatment.

Consequently, inhibition of Brg1 decreased gammaherpesviral lytic reactivation. Here we demonstrate how gammaherpesviruses hijack the function of two host proteins to promote their lytic replication cycle.

Overall, this study provided new insights into DDX17-mediated pro-inflammatory chemokine activation, which unveiled the association between DDX17 and β-catenin/ NF-κB complex in transactivating the expression of CXCL8. The usage of CXCR1/2 inhibitor to block DDX17-induced CXCL8 signaling activation might be a potential therapeutic approach for HCC treatment.

PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.