DHX9 (DExH-Box Helicase 9)

TDG inhibition in p53-deficient cancer cells leads to DHX9 downregulation and, thus, aberrant dsRNA accumulation, which activates the RIG-I/MDA5-MAVS sensing pathway, resulting in tumor suppression and enhanced antitumor immunity. These findings highlight the synthetic lethality between TDG and p53, positioning TDG inhibition as a promising therapeutic strategy for p53-deficient cancers.

Our findings reveal that LFQSNY laser inhibits the melanogenesis of melanocytes and enhances the effect of anti-inflammation for improves pigment-clearance in melasma via a non-thermal photobiomodulation. The insights provide a mechanistic rationale for enhancing clinical efficacy of LFQSNY laser-therapy in melasma.

Our study discovers that DHX9 promotes AML development and may serve as a biomarker for AML, holding a better prospect for clinical application.

Importantly, the tumor-suppressive effect of DHX9 knockdown was reversed by BECN1 downregulation. In conclusion, the previously unrecognized significance of DHX9 in mediating the epigenetic silencing of BECN1, which is essential for autophagy and tumorigenesis, highlights its potential as an effective biomarker as well as a prospective therapeutic candidate for BC.

Haprolid inhibits the AKT signaling pathway by downregulating DHX9, ultimately suppressing HCC growth. This finding opens up new avenues for targeted HCC therapy.

AURKB overexpression promotes the malignant phenotype of osteosarcoma cells by activating the NF-κB signaling pathway via regulating DHX9.

This review emphasizes the diverse roles of CARMN across different cancers and its potential as a diagnostic and therapeutic tool. Future research should address the mechanistic details of CARMN's involvement in cancer, validate its clinical utility, and explore its therapeutic potential in combination with existing treatments.

ATX968 was identified as a potent and selective inhibitor of DHX9 helicase activity...These preclinical data validate DHX9 as a target for the treatment of patients with MSI-H/dMMR. Additionally, this potent and selective inhibitor of DHX9 provides a valuable tool with which to further explore the effects of inhibition of DHX9 enzymatic activity on the proliferation of cancer cells in vitro and in vivo.

Moreover, DHX9 was upregulated in tumors from PARPi-resistant BRCAm HGSOC patients, and high co-expression of DHX9 and AKT1 correlated with worse survival. Together, this study reveals an interaction between AKT1 and DHX9 that facilitates R-loop resolution and identifies combining ATRi and AKTi as a rational treatment strategy for BRCAm HGSOC irrespective of PARPi resistance status.

Conversely, EWS-FLI1 binding to the promoter represses YAP1 expression. These findings identify the DHX9/KDM2B complex as a new druggable target to counteract ES malignancy.

BAP1 is the most solid biomarker of a poor prognosis in UM and mutations can be detected using NGS. SF3B1 is associated with the spindle cell subtype of UM, which gives it probably a favourable prognostic value. Our study suggests that mutations in DHX9 and PDK1 can have prognostic value. These potential biomarkers are related to the PI3K/AKT/mTOR pathway and makes them candidates for developing new directed therapies.