Sep 18, 2018 · Depletion of DDX5 could promote HCC cells growth. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that PI3K/Akt signaling pathway obtained the highest enrichment. Furthermore, we found that knockdown of DDX5 decreased Akt as well as p-Akt (S473) expressions.

DDX5 (p68) is a well-known multifunctional DEAD-box RNA helicase and a transcription cofactor. Since its initial discovery more than three decades ago, DDX5 is gradually recognized as a potential biomarker and target for the treatment of various cancer types.

Jan 1, 2019 · Direct evidence of the role of DDX5 in the tumorigenesis of colon cancer is presented by recent studies reporting that the overexpression of DDX5 positively regulates the AKT signaling pathway.

OGT-mediated O-GlcNAcylation stabilizes DDX5, activates the AKT/mTOR signaling pathway, and then accelerates the progression of colorectal cancer . Protein arginine methyltransferase 5 methylates the RGG/RG motif in the C-terminal of DDX5.

Aug 19, 2023 · In this review, we discuss the multifaceted functions of DDX5 in DNA repair in cancer, immune suppression, oncogenic metabolic rewiring, virus infection promotion, and negative impact on the human microbiome (microbiota).

The increase in AKT transcription coupled with the depletion of the tumor suppressor FOXO3a (a downstream gene) accounts for the oncogenic role of DDX5 in colon cancer. In addition, DDX5 also regulates the expression of RelA, a component of the NF-κB signaling pathway, which is involved in colon tumorigenesis [ 64 ].

DDX5 deficiency orchestrates the activation of Wnt/β-catenin signaling in sorafenib-treated cells, thereby mediating escape from ferroptosis, a mechanism linked to drug resistance in cancer

Furthermore, we found that knockdown of DDX5 decreased Akt as well as p-Akt (S473) expressions. Collectively, these findings suggested that DDX5 facilitated HCC cells growth via Akt signaling pathway.

Mechanistically, circEGFR acted as a ceRNA for miR-106a-5p to relieve the repressive effect of miR-106a-5p on DDX5 mRNA. Moreover, circEGFR enhanced DDX5 expression, thereby upregulating p-AKT levels.

Here, we show that the DEAD box RNA helicase 5 (DDX5) is overexpressed in alveolar RMS cells and that its depletion and pharmacological inhibition decrease FP-RMS viability and slow tumor growth in xenograft models.