DDX58 (DExD/H-Box Helicase 58)

In summary, this study elucidates the biological functions of DDX60 in CRC and provides novel experimental evidence supporting its potential as a therapeutic biomarker.

Syrosingopine treatment sensitizes LUAD cells to PARP inhibitor (PARPi) and potentiates the therapeutic efficacy of olaparib in a mouse LUAD model. Altogether, our study reveals that lactylation drives RIG-I nuclear function to inhibit DNA damage repair via PARP suppression. This supports the potential co-administration of syrosingopine and PARPi for LUAD treatment.

We recently completed a clinical trial in dogs with DLBCL using a combination of canine anti-CD20 antibody and low dose doxorubicin followed by one of three small molecule immune-modulating agents (KPT-9274, TAK-981 or RV1001). To facilitate point-of-care PBMC gene expression testing that could be used to distinguish those dogs likely to require more intensive treatment regimens in advance of relapse, we developed qPCR assays for TBHD, NPNT and ISG20 . Together these data provide proof of principle that biomarker interrogation in PBMCs can help predict early relapse and poor responders to inform clinical management of DLBCL.

Through a series of analyses, we speculate that these hub genes can serve not only as combined biomarkers for predicting responses to multiple therapies but also as novel molecular targets for the development of synergistic treatment strategies via their mediated immune microenvironment interactions. These findings provide a new translational research direction for overcoming therapeutic resistance in cervical cancer.

The degradation of DDX58 by TRIM6 alleviates its inhibitory effects on Snail1, thereby facilitating EMT and enhancing the invasive potential of HCC cells. These findings establish the STAT3-TRIM6-DDX58-Snail1 axis as a pivotal pathway in HCC progression, offering novel insights into the molecular underpinnings of HCC metastasis and highlighting TRIM6 as a potential therapeutic target and prognostic biomarker in HCC.

In addition, gene network analysis highlighted CCNA2, CDK1, DDX58, DHX58, EXO1, GBP1, IFIH1, IFIT1, IFIT2, IFIT3, IRF7, ISIG15, MX1, OAS1, OAS2, PARP9, TOP2A and XAF1 as potential hub genes influencing the response of CCA cells to NDV LaSota strain. Our findings offer evidence supporting the promise of NDV-based therapies as potential strategies for eliminating CCA cells.

In this study, we found that RNF157 is a tumour-promoting ubiquitin ligase that promotes liver cancer growth by targeting RIG-I/DDX58 for degradation. Thus, RNF157 has the potential to be a therapeutic target for liver cancer.

A critical mechanism for the protumor immune microenvironment mediated by therapy-induced senescent glioblastoma cells, the DDX58-STAT1-CSF1 axis, may be a potential therapeutic avenue for alleviating traditional therapy-induced glioblastoma cell senescence.

We demonstrate that METTL3 depletion induces a chronic antiviral state that dramatically inhibits viral replication. Our study is important for understanding and improving oncolytic virus-based therapies.

Overall, our results implied that RNF135 promotes the stemness of breast cancer cells by ubiquitinating and degrading DDX58 and targeting of RNF135/DDX58 axis might be a feasible method to suppress tumorigenesis and metastasis of breast cancer patients.

Remarkably, the neural network model demonstrated exceptional diagnostic accuracy in distinguishing between the disease states (DLBL and SLE) based solely on the expression patterns of these hub genes. The identified hub genes and their associated pathways hold immense potential as diagnostic biomarkers and may serve as valuable targets for future therapeutic explorations.

Conversely, in SK-N-AS cells, IFI27 overexpression inhibited cell proliferation, migration, and invasion. IFI27 was lowly expressed in NB and participated in the progression of NB, which provides a new insight into the pathogenic mechanism and novel therapeutic strategy for NB.