Interleukin-24 Suppresses the Growth of Vascular Smooth Muscle Cells by Inhibiting H&lt;sub&gt;2&lt;/sub&gt;O&lt;sub&gt;2&lt;/sub&gt;-Induced Reactive Oxygen Species Production

Lee, Ki-Mo; Kang, Haeng-A; Park, Min; Lee, Hwa-Youn; Song, Min-Ji; Ko, Kisung; Oh, Jae-Wook; Kang, Hyung‐Sik

doi:10.1159/000343242

Cited by 13 publications

(10 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3A). Our results are also supported by the recent reported observation that recombinant human IL-24 protein induced a cell cycle arrest at the G 0 /G 1 phase through the downregulation Cyclin D1 in MOVAS cells [51]. Together, these data indicate that the downregulation of Cyclin D1 is caused, at least partially, by SC144-induced upregulation of IL-24, and results in cell cycle arrest.…”

Section: Sc144 Causes Cell Cycle Arrestsupporting

confidence: 91%

Stabilization of MDA-7/IL-24 for colon cancer therapy

Oshima

Imada

et al. 2013

Cancer Letters

View full text Add to dashboard Cite

Section: Sc144 Causes Cell Cycle Arrestsupporting

confidence: 91%

Stabilization of MDA-7/IL-24 for colon cancer therapy

Oshima

Imada

et al. 2013

Cancer Letters

View full text Add to dashboard Cite

“…Ectopic expression of Bcl-2 and Bcl-XL inhibited Ad-IL24 induced mitochondrial changes, ROS production and apoptosis, which further substantiates the involvement of mitochondrial dysfunction in Ad-IL24 induced apoptosis [41]. In contrast to these findings, Lee et al reported IL-24 inhibited hydrogen peroxide (H 2 O 2 ) induced ROS production in normal vascular smooth muscle cells (VSMC) by reducing mitochondrial H 2 O 2 production and by enhancing the expression of antioxidant enzymes [46]. It is evident from these reports that IL-24 selectively induces ROS-mediated cell death in tumor cells but not in normal cells.…”

Section: Reviewmentioning

confidence: 75%

Molecular targets and signaling pathways regulated by interleukin (IL)-24 in mediating its antitumor activities

Panneerselvam

Munshi

Ramesh

2013

JMS

View full text Add to dashboard Cite

Cancer remains a major health issue in the world and the effectiveness of current therapies is limited resulting in disease recurrence and resistance to therapy. Therefore to overcome disease recurrence and have improved treatment efficacy there is a continued effort to develop and test new anticancer drugs that are natural or synthetic - (conventional chemotherapeutics, small molecule inhibitors) and biologic (antibody, tumor suppressor genes, oligonucleotide) product. In parallel, efforts for identifying molecular targets and signaling pathways to which cancer cells are “addicted” are underway. By inhibiting critical signaling pathways that is crucial for cancer cell survival, it is expected that the cancer cells will undergo a withdrawal symptom akin to “de-addiction” resulting in cell death. Thus, the key for having an improved and greater control on tumor growth and metastasis is to develop a therapeutic that is able to kill tumor cells efficiently by modulating critical signaling pathways on which cancer cells rely for their survival.Currently several small molecule inhibitors targeted towards unique molecular signaling pathways have been developed and tested in the clinic. Few of these inhibitors have shown efficacy while others have failed. Thus, targeting a single molecule or pathway may be insufficient to completely block cancer cell proliferation and survival. It is therefore important to identify and test an anticancer drug that can inhibit multiple signaling pathways in a cancer cell, control growth of both primary and metastatic tumors and is safe.One biologic agent that has the characteristics of serving as a potent anticancer drug is interleukin (IL)-24. IL-24 suppresses multiple signaling pathways in a broad-spectrum of human cancer cells leading to tumor cell death, inhibition of tumor angiogenesis and metastasis. Additionally, combining IL-24 with other therapies demonstrated additive to synergistic antitumor activity. Clinical testing of IL-24 as a gene-based therapeutic for the treatment of solid tumors demonstrated that IL-24 is efficacious and is safe. The unique features of IL-24 support its further development as an anticancer drug for cancer treatment.In this review we summarize the current understanding on the molecular targets and signaling pathways regulated by IL-24 in mediating its anticancer activity.

show abstract

“…This research suggested that IL-24 may be a potential therapeutic agent in the calcification of VSMCs. Beides this, another study demonstrated that IL-24 suppressed the growth of normal VSMCs by inhibiting H 2 O 2 -induced ROS production through the regulation of mitochondrial ROS production and the expression of antioxidant enzymes ( 44 ). In a recent study, the researchers found that IL-24 polymorphisms were associated with cardiometabolic parameters and cardiovascular risk factors ( 45 ).…”

Section: Discussionmentioning

confidence: 99%

The IL-24 gene protects human umbilical vein endothelial cells against H2O2-induced injury and may be useful as a treatment for cardiovascular disease

Wang

Chen

et al. 2016

International Journal of Molecular Medicine

View full text Add to dashboard Cite

The aim of the present study was to investigate the protective effects of interleukin-24 (IL-24) on hydrogen peroxide (H2O2)-induced vascular endothelial injury and to examine the association between IL-24 and cardiovascular disease. Human umbilical vein endothelial cells (HUVECs) were exposed to increasing concentrations of H2O2 in the presence or absence of IL-24, which was introduced via Lipofectamine® 2000-mediated transfection. The successful uptake of the IL-24 plasmid was confirmed by RT-PCR at 24 h post-transfection. The effects of H2O2 and IL-24 on the proliferation and migration of the HUVECs was determined using cell migration assays. Cell viability was determined using a Cell Counting Kit-8 (CCK-8). Apoptosis and the measurement of the intracellular reactive oxygen species (ROS) levels were determined by flow cytometry, and the levels of caspase-3, which is associated with apoptosis, were determined by western blot analysis. Real-time PCR and western blot analysis were also used to measure the levels of multiple cardiovascular disease-associated factors. In vivo experiments were also performed using a rat model of hypertension which was constructed by angiotensin II infusion using an osmotic pump. The mRNA and protein levels of IL-24 were measured in both the control and hypertensive rats; the effects of treatment with enalapril and nifedipine on the IL-24 levels were also examined. Our results revealed that IL-24 protected against the H2O2-mediated abnormal increase in HUVEC proliferation. IL-24 also antagonized H2O2 by reducing the content of ROS in the cells, thus decreasing cellular oxidative damage, improving the cellular survival rate, reducing apoptosis and decreasing the expression of cardiovascular disease-related factors. The results from our in vivo animal experiments revealed that IL-24 expression was lower in the hypertensive rats compared to the healthy controls. Additionally, the IL-24 levels increased following anti-hypertensive therapy. The findings of our study indicate that IL-24 protects against H2O2-mediated endothelial cell damage and may thus provide a novel therapeutic strategy for treatment of cardiovascular disease.

show abstract

Interleukin-24 Suppresses the Growth of Vascular Smooth Muscle Cells by Inhibiting H<sub>2</sub>O<sub>2</sub>-Induced Reactive Oxygen Species Production

Cited by 13 publications

References 26 publications

Stabilization of MDA-7/IL-24 for colon cancer therapy

Stabilization of MDA-7/IL-24 for colon cancer therapy

Molecular targets and signaling pathways regulated by interleukin (IL)-24 in mediating its antitumor activities

The IL-24 gene protects human umbilical vein endothelial cells against H2O2-induced injury and may be useful as a treatment for cardiovascular disease

Contact Info

Product

Resources

About