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cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) activation is required for IL-24-induced cell death in a variety of breast cancer cell lines.
Results show that iron-induced calcification in vascular smooth muscle cells occurred via IL-24; IL-24 was increased during the calcification process induced by iron, and IL-24 itself caused calcification in the absence of iron. These results confirmed the role of interleukin-24 as a candidate gene that might contribute to calcification in vascular media cells.
These results indicated that low expression of Mda-7/IL-24 along with high expression of C-myb are predictors for poor prognosis of Burkitt lymphoma patients; this outcome suggests that Mda-7/IL-24 and C-myb might be potential targets for clinical treatment of Burkitt lymphoma.
Secretome analysis revealed that Oct4 upregulated interleukin 24 (IL24) expression through STAT3 and NFkappaB signaling, and siRNA against IL24 increased IRinduced senescence, whereas recombinant human IL24 suppressed it. The results of the present study indicated that Oct4 confers IR resistance on breast cancer cells by suppressing IRinduced premature senescence through STAT3- and NFkappaB-mediated IL24 production.
These results suggest that hIL-24 can reverse the cisplatin (DDP)- resistance of lung cancer cells, and that the associated mechanism involves the induction of apoptosis and G2/M-phase arrest through the phosphoinositide3-kinase (PI3K)/AKT signaling pathway, as well as a decrease in drug resistance through P-gp expression
These results indicated that Mda7/IL24 could induce terminal differentiation of B lymphoma cells by regulating the expression of Blimp1 and Bcl6 via altering the P38 MAPK signaling pathway.
These results demonstrate a previously unrecognized role of IL24 in inhibition of translation, mediated through both phosphorylation of eIF2alpha and dephosphorylation of 4E-BP1, and provide the first direct evidence for translation control of gene-specific expression by IL24
IL-24 inhibits AKT via regulating the HMGA1/miR-222 signaling node in human lung cancer cells and acts as an effective tumor suppressor.
this paper shows that IL-24 represents a potential biomarker of allergic inflammation and a Th2 polarized condition of the epithelium
Low IL24 expression is associated with endometriosis.
IL-20 and IL-24 increased the production of monocyte chemoattractant protein-1 by activated spondyloarthritis synovial fluid monocytes, decreased the production of Dickkopf-1 by SpA fibroblast-like synovial cells and induced mineralization in human osteoblasts; taken together, findings indicate disease-aggravating functions of IL-20 and IL-24 in spondyloarthritis
a novel pathway for mda-7/IL-24-induced caspase-independent apoptosis in neuroblastoma cells mediated through modulation of AIF, ATM, and gamma-H2AX.
mda-7/IL-24 directly regulates miRNA expression in cancer cells and highlights the novelty of the mda-7/IL-24-miR-221-beclin-1 loop in mediating cancer cell-specific death.
LINC00152-mediated oncogenic effects occur in part through the epigenetic silencing of IL24 expression following binding with EZH2.
mechanistic studies, inhibition of SRC and PKCdelta completely ablated the ability of MDA-7/IL-24 to reduce the Bcl-x(L)/(s) mRNA ratio and cell viability. These findings show that Bcl-x(s) expression is an important mediator of MDA-7/IL-24-induced cytotoxicity requiring the SRC/PKCdelta signaling axis in NSCLC cells.
Expression of IL-24 and IGFBP-3 significantly suppressed prostate cancer tumor growth in vivo.
Results suggest that IL-24 exerts a potent suppressive effect on influenza viral replication and can be used in the treatment of influenza infection.
Expression of IL-24 enhanced the sensitivity of B lymphoma cells to chemotherapy agents by altering the expression of multidrug-resistance genes via downregulating GTP-RhoA-ERK signaling pathway
IL20R1 correlated with prognosis of patients with pancreatic cancer, and mediates pancreatic cancer cell growth and migration. It may be a potential biomarker for IL24 molecular-targeted therapy.
The anti-viral effect of IL-24 correlated with caspase-3 activation and could be blocked by a pan-caspase inhibitor and by small interfering RNA (siRNA) directed towards TLR3.
Despite being coexpressed, IL-10 and IL-24 are independently regulated by different type I IFN receptor signaling pathways.
our data suggest that IL-20 subfamily cytokines, particularly IL-20, IL-22, and IL-24, might provide therapeutic benefit for patients with Diabetic foot ulcers (DFU) .
this study shows that IL-24 promotes Pseudomonas aeruginosa keratitis through the suppression of early protective mucosal immunity
Loss of IL-24 expression is associated with breast cancer.
A psoriasis-like skin inflammation in mice with epidermis-specific inhibition of NF-kappaB was triggered by TNFR1-dependent upregulation of interleukin-24 & activation of STAT3 signaling in keratinocytes.
IL-24 suppresses the growth of normal vascular smooth muscle cells by inhibiting hydrogen peroxide-induced reactive oxygen species (ROS) production through the regulation of mitochondrial ROS production and expression of antioxidant enzymes
Secretory mIL-24 did not induce the expression of the IL-6, TNF-alpha or IFN-gamma gene in spleen cells
T cell receptor stimulation induces IL-24 expression in T helper type (Th)2 cells by the coordinate action of Stat6 and c-Jun transcription factors at the transcriptional level.
induction of Il24 by oncogenes may support tumor growth at the early stages of cancer
Grp170 enhances therapeutic activity of a novel tumor suppressor, mda-7/IL-24
the novel splicing variant of IL24, FISP-sp dimerizes with FISP and blocks its secretion and inhibits FISP-induced apoptosis in vivo
Data demonstrated that IL-24 predominately stimulated neutrophils to produce IFN-gamma and IL-12, subsequently activating CD8+ T cells both in vivo and in vitro.
This gene encodes a member of the IL10 family of cytokines. It was identified as a gene induced during terminal differentiation in melanoma cells. The protein encoded by this gene can induce apoptosis selectively in various cancer cells. Overexpression of this gene leads to elevated expression of several GADD family genes, which correlates with the induction of apoptosis. The phosphorylation of mitogen-activated protein kinase 14 (MAPK7/P38), and heat shock 27kDa protein 1 (HSPB2/HSP27) are found to be induced by this gene in melanoma cells, but not in normal immortal melanocytes. Alternatively spliced transcript variants encoding distinct isoforms have been reported.
IL-4-induced secreted protein
, melanocyte-associated Mda-7
, melanoma differentiation-associated gene 7 protein
, suppression of tumorigenicity 16 (melanoma differentiation)
, th2-specific cytokine FISP
, cytokine-like protein Mob-5
, interleukin 24