DDX10 (DEAD-Box Helicase 10)

DDX10 contributes to the proliferation and invasion of DLBCL cells via positively regulating FBL, highlighting the DDX10-FBL axis as a potential therapeutic target. This work provides new insights into DLBCL pathogenesis and underscores the biomedical relevance of targeting DDX10-FBL.

Collectively, our findings indicate that DDX10 promotes PC cell proliferation primarily by upregulating RRM2, thus highlighting its potential as a promising therapeutic target in PC.

PPPET has unique morphologic, immunohistochemical, and molecular genetic characteristics. Our findings suggest that PPPET may be an independent neurooncological entity.

These findings highlight that the oncogenic role of DDX10 in promoting exosomal PD-L1 secretion via phase separation with Rab27b has been preliminarily validated in T cell exhaustion in OSCC. A potential strategy for improving OSCC immunotherapy may involve the inhibition of DDX10.

However, its activity can be inhibited by several factors, including DDX10, PTBP1, sodium orthovanadate, podofilox, SIRT6, FAT1, SOX2 and multiple microRNAs (e.g., miR-369-3p, miR-100-3p, miR-27b-3p, miR-197-3p, let-7i-5p and miR-552). This review explores the functional and clinical significance of ATG10 across various cancers, highlighting its potential as a biomarker and therapeutic target.

Involvement of genetic variants in the initiation, diagnosis and prognosis of myelodysplastic syndrome was noted.

We also identified a novel function of NOL10 in that it acts cooperatively with NUP98::DDX10 to regulate serine biosynthesis pathways and stabilize ATF4 mRNA. Collectively, these findings suggest that NOL10 is a critical regulator of NUP98::DDX10 leukemia and that targeting NOL10 (or the serine synthesis pathway regulated by NOL10) may be an effective therapeutic approach.

An in vivo xenograft assay further confirmed the therapeutic potential of compound 5o, demonstrating tumor growth inhibition rates of 60%, 78%, and 88% at doses of 5 mg/kg, 10 mg/kg, and 20 mg/kg, respectively. This study highlights a promising chemotherapeutic agent for the effective treatment of lung cancer.

Notably, the NUP98-DDX10 fusion associated with acute myelocytic leukemia (AML) alters the cellular localization of DDX10 and results in loss of ability to regulate pre-rRNA processing. Collectively, this study reveals the critical role of DDX10 as a pivotal regulator of ribosome biogenesis in mESCs.

Our study revealed the clinical and genetic characteristics of patients with myeloid neoplasms harboring rare and non-cryptic NUP98r. Given its association with poor prognosis, a comprehensive evaluation is crucial for identifying previously underdiagnosed NUP98r in patients with myeloid neoplasms.

Consequently, ATG10 depletion or treatment with autophagy inhibitor 3-Methyladenine (3-MA) partially compensated the influences of DDX10 silencing on the proliferation, apoptosis and stemness of CRC cells. Accordingly, DDX10 deficiency may aggravate autophagy mediated by ATG10 to impede cell proliferation, stemness and facilitate cell apoptosis, hence blocking the progression of CRC.

Four signature-related genes could relatively precisely predict the prognosis of patients with PDAC. Specifically, DDX21 upregulation may signal an unfavorable prognosis by negatively affecting the biological properties of PDAC cells. DDX21 may be considered as a candidate therapeutic target in PDAC.