DDX5 (DEAD-Box Helicase 5)

In a subcutaneous tumor model, in which Ba/F3 cells expressing JAK2V617F and EpoR were transplanted into nude mice, oral administration of FL118 significantly reduced tumor growth and hepatosplenomegaly. Collectively, these findings establish DDX5 as a promising therapeutic target in MPNs and underscore the potential of FL118 as a treatment strategy for JAK2V617F-driven disease.

Collectively, low expression of RNF125 predicted poor prognosis of NSCLC patients. Upregulation of RNF125 repressed proliferation, mobility, invasion and stemness of NSCLC through the ubiquitinated degradation of DDX5.

Elevated expression of CPSF73 is associated with aggressive disease in prostate cancer patients, and combining JTE-607 with adavosertib synergistically reduced prostate cancer cell survival. Our findings suggest that transcription termination helps prevent toxic conflicts between transcription and replication following increased replication initiation caused by WEE1 inhibition.

Placental gene expression differences between nulliparas and multiparas may in part underlie neonatal outcomes that differ by parity and fetal sex.

Knockdown of DDX5 in A3C-proficient H1299 cells attenuated gemcitabine-induced Chk1 activation and enhanced the therapeutic index of gemcitabine by promoting R-loop accumulation. Therefore, we conclude that A3C/DDX5/R-loop complex may impair the sensitivity of gemcitabine by modulating Chk1 dynamics and DNA replication/damage response machinery.

Metabolite profiling revealed that the introduction of difluoro substitution effectively reduced metabolic risk. Collectively, A10 represents a promising candidate for further preclinical development against colorectal cancer.

P1, N=340, Recruiting, Shanghai Henlius Biotech | N=174 --> 340

Furthermore, DDX5 facilitates mechanistic target of rapamycin (mTOR) signaling, thereby promoting the proliferation and tumorigenic potential of MPN cells...These findings demonstrate that the RNA helicase activity of DDX5 is dispensable for JAK2V617F-induced transformation. These findings suggest that DDX5 promotes oncogenesis through helicase-independent mechanisms and represents a potential therapeutic target in JAK2V617F-driven malignancies.

ZC3H12D and DDX5 are a pair of cell cycle antagonists in breast cancer that inhibit or promote the cell cycle progression by modulating the expression of cell cycle-promoting genes, which provide new insights into the prevention of uncontrolled cancer cell cycle transitions.

Genetic or pharmacological degradation of RBM39 (using the clinically explored molecular glue indisulam) potently reactivates latent HIV-1 in J-Lat cell models, primary CD4⁺ T cells from people living with HIV-1 (PLWH), and synergizes with established LRAs (Bryostatin-1, JQ-1, SAHA) to broadly activate proviral reservoirs...In addition to establishing RBM39 as a promising therapeutic target for addressing the limitations of current "shock and kill" strategies, our findings establish a novel mechanistic framework for m⁶A-dependent regulation of viral gene expression. This framework may serve as a valuable reference for investigating similar regulatory mechanisms in other latent viral infections or oncogenic processes where RNA methylation plays a pivotal role.

Furthermore, our findings clarified that DDX5 and eEF1A2 mediated the stimulative function of SYVN1 in ESCC progression and NF-κB pathway was responsible for the effects of SYVN1/DDX5/eEF1A2 axis on ESCC. Overall, this study illustrated that SYVN1 promoted the M2 polarization of TAMs to induce ESCC progression by targeting DDX5 and eEF1A2 to activate NF-κB pathway.

However, the analysis of patient-derived tumor samples revealed a positive correlation between p65 and p68, underscoring their clinical relevance. Hence, our findings elucidate novel transcriptional feedback "p65-68 loop" and its therapeutic potential in CRC and glioma.