Table 2.

Role of DDX5 in cancer.

Cancer	Role 1	Mechanism	Ref.
Colorectal	+	DDX5 overexpression promotes cancer by AKT/mTOR signaling or association with AldoA	[62,63,64,65,66]
Breast	+	upregulates a subset of miRNAs; highly correlated with Ki67; involved in β-catenin/Wnt pathway	[67,68,69]
Leukemia	+	DDX5 depletion selectively induces stress in AML cells; positive regulator of NOTCH1 signaling; DDX5 inhibition reduces tumor proliferation	[70,71,72]
Non-small-cell lung/small cell lung	+	induces β-catenin to promote cell proliferation	[73,74]
Osteosarcoma	+	lncRNA DLEU1/miR-671-5p/DDX5 interaction to promote cancer progression	[75]
Prostate	+	lncRNA CCAT1/DDX5/miR-28-5p interaction to promote cancer progression; DDX5-ETV4 fusion protein	[76,77]
Gastric	+	high DDX5 expression activates mTOR/SK61 pathway to induce cancer progression; lnc MIAT interaction	[78,79]
Glioblastoma	+	NF-κB p50 subunit activation; lncRNA LINC01116 interaction; hyperactivation of ERK and downregulation of DUSP5	[80,81,82]
Cervical	+	stimulation of the expression of TGF-β1 in CaSki cells	[83]
Endometrial	+	HDGF/DDX5 interaction to induce β-catenin	[84]
Squamous cell carcinoma (HNSCC)	+	high DDX5 expression is associated with cancer progression	[85]
Squamous cell carcinoma (ESCC)	+	decreased DDX5 expression is associated with inhibition of cancer progression	[86]
Human hepatocellular carcinoma (HCC) associated with HBV	−	inhibits cancer progression by interacting with p62/SQSTM1, by regulation of miRNAs and by associating with lncRNA HOTAIR	[87,88,89,90,91]

¹ Oncogene (+), oncosuppressor (−).