Coexpression of growth differentiation factor 11 and reactive oxygen species in metastatic oral cancer and its role in inducing the epithelial to mesenchymal transition

Qin, Xiangming; Kuang, Hai; Chen, Lei; Wei, Shanliang; Yu, Dahai; Liang, Feixin

doi:10.1016/j.oooo.2017.03.010

Cited by 29 publications

(18 citation statements)

References 37 publications

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“…Additionally, accumulating evidence suggests that Nox, the major source of ROS in the cardiovascular system, is an important downstream effector of the TGF-β signaling pathway, whereas Nox-dependent redox signaling regulates TGF-β/Smad signaling in a feedforward manner (46). Qin et al (47) reported that GDF11 overexpression and ROS overproduction was observed in patients with metastatic oral cancer; however, treatment with the antioxidant, N-acetylcysteine, suppressed the GDF11-induced epithelial-mesenchymal transition and migration of tumor cells. Of note, the present study demonstrated that ISO treatment induced oxidative stress injury, reflected by increased ROS and MDA concentrations, which was exacerbated by rGDF11 treatment in ISO-treated H9C2 cells.…”

Section: Discussionmentioning

confidence: 99%

Growth differentiation factor 11 is involved in isoproterenol‑induced heart failure

et al. 2019

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The present study aimed to investigate the potential effects of growth differentiation factor 11 (GDF11) on isoproterenol (ISO)-induced heart failure (HF) and identify the underlying molecular mechanisms. A rat model of HF was induced in vivo by intraperitoneally administering ISO (5 mg/kg/day) for 7 days. After 4 weeks following establishment of the HF model, hemodynamic analysis demonstrated that ISO induced a significant increase in the left ventricular end-diastolic pressure and a decrease in the left ventricular systolic pressure and maximum contraction velocity. The plasma levels of myocardial injury markers, including lactate dehydrogenase (LDH), creatine kinase (CK), CK-muscle/brain which were determined using the corresponding assay kits and plasma brain natriuretic peptide which was detected by an ELISA kit, an important biomarker of HF, increased following ISO treatment. Furthermore, levels of GDF11 expression and protein, which were estimated using reverse transcription-quantitative polymerase chain reaction and an ELISA kit in plasma and western blotting in the heart tissue, respectively, significantly increased following ISO treatment. To demonstrate the effects of ISO on GDF11 production in cardiomyocytes, H9C2 cells (a cardiomyoblast cell line derived from embryonic rat heart tissue) were treated with ISO (50 nM) for 24 h in vitro ; it was revealed that GDF11 protein and mRNA expression levels significantly increased following ISO treatment. In addition, recombinant GDF11 (rGDF11) administered to ISO-treated H9C2 cells resulted in decreased proliferation, which was detected via a CCK-8 assay, and increased LDH levels and cell apoptosis of cells, which was determined using Caspase-3 activity and Hoechst 33258 staining. Additionally, rGDF11 increased the levels of reactive oxygen species and malondialdehyde due to the upregulation of nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) following rGDF11 treatment. Conversely, GDF11 knockdown reduced ISO-induced apoptosis by inhibiting oxidative stress injury. The results suggested that GDF11 production was upregulated in ISO-induced rats with HF and in ISO-treated H9C2 cells, and that rGDF11 treatment increased ISO-induced oxidative stress injury by upregulating Nox4 in H9C2 cells.

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Section: Discussionmentioning

confidence: 99%

Growth differentiation factor 11 is involved in isoproterenol‑induced heart failure

et al. 2019

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“…ROS is highly involved in the cancer progression, which is a complicated process that includes uncontrolled proliferation and apoptosis resistance, migration and invasion of tumor cells, and angiogenesis around the tumor lesion [ 31 , 35 ]. Previous studies demonstrated that ROS was excessively produced in oral cancer [ 36 , 37 ]. Accordingly, we found that high amounts of ROS were generated in oral cancer cells and tumor xenografts.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Inhibits Reactive Oxygen Species‐Driven Proliferation, Epithelial‐Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer

Wang

Deng

et al. 2018

Oxidative Medicine and Cellular Longevity

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Globally, oral cancer is the most common type of head and neck cancers. Melatonin elicits inhibitory effects on oral cancer; however, the biological function of melatonin and underlying mechanisms remain largely unknown. In this study, we found that melatonin impaired the proliferation and apoptosis resistance of oral cancer cells by inactivating ROS-dependent Akt signaling, involving in downregulation of cyclin D1, PCNA, and Bcl-2 and upregulation of Bax. Melatonin inhibited the migration and invasion of oral cancer cells by repressing ROS-activated Akt signaling, implicating with the reduction of Snail and Vimentin and the enhancement of E-cadherin. Moreover, melatonin hampered vasculogenic mimicry of oral cancer cells through blockage of ROS-activated extracellular-regulated protein kinases (ERKs) and Akt pathways involving the hypoxia-inducible factor 1α. Consistently, melatonin retarded tumorigenesis of oral cancer in vivo. Overall, these findings indicated that melatonin exerts antisurvival, antimotility, and antiangiogenesis effects on oral cancer partly by suppressing ROS-reliant Akt or ERK signaling.

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“…In additional, MICAL1 overexpression induces reactive oxygen species (ROS) generation and increases Akt phosphorylation in breast cancer cell 7 . ROS can induce the metastasis and invasion of cancer cells by epithelial-mesenchymal transition (EMT) 8 - 10 . MICAL-L2 protein is upregulated in ovarian cancer by Wnt/β-catenin pathway, and the silencing of MICAL-L2 is correlated with the decrease of SNAIL, TWIST, ZEB1 and ZEB2 11 , which are the transcription factors of EMT 12 .…”

Section: Introductionmentioning

confidence: 99%

Overexpression of MICAL2, a novel tumor-promoting factor, accelerates tumor progression through regulating cell proliferation and EMT

Cai

Tang

2018

J. Cancer

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Molecule interacting with CasL 2 (MICAL2), a microtubule associated monooxygenase, is involved in cell growth, axon guidance, vesicle trafficking and apoptosis. Recent studies have demonstrated that MICAL2 is highly expressed in tumor and accelerates tumor progression and it is deemed to be a novel tumor-promoting factor. MICAL2 overexpression increases cell proliferation to accelerate tumor growth, and MICAL2 also promotes epithelial-mesenchymal transition (EMT)-related proteins to increase cancer cell metastasis. On mechanism, MICAL2 induces EMT by regulating SRF (serum response factor)/MRTF-A (myocardin related transcription factor A) signaling, Semaphorin/Plexin pathway and inducing ROS (Reactive oxygen species) production. In the present review, we introduced MICAL family, expatiated the structure and functions of MICALs, and summarized the mechanisms of MICAL2 involving tumor progression. The challenges and perspectives for MICAL2 in tumor are also discussed.

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Coexpression of growth differentiation factor 11 and reactive oxygen species in metastatic oral cancer and its role in inducing the epithelial to mesenchymal transition

Cited by 29 publications

References 37 publications

Growth differentiation factor 11 is involved in isoproterenol‑induced heart failure

Growth differentiation factor 11 is involved in isoproterenol‑induced heart failure

Melatonin Inhibits Reactive Oxygen Species‐Driven Proliferation, Epithelial‐Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer

Overexpression of MICAL2, a novel tumor-promoting factor, accelerates tumor progression through regulating cell proliferation and EMT

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