H<sub>2</sub>O<sub>2</sub>Inhibits Proliferation and Mediates Suppression of Migration via DLC1/RhoA Signaling in Cancer Cells

Ma, Long; Zhu, Wenzhen; Liu, Tingting; Fu, Huiling; Liu, Zhaojun; Yang, Bingwu; Song, Taiyu; Li, Guorong

doi:10.7314/apjcp.2015.16.4.1637

Cited by 22 publications

(17 citation statements)

References 32 publications

(34 reference statements)

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“…In the present study, increased excretion of ROMO1 and ROS was not observed in blood serum in the UUO model. Furthermore, H 2 O 2 is regarded as an important element that influences cellular proliferation ( 31 ). In the present study, the expression of ROMO1 was upregulated when the HK-2 cell line was treated with H 2 O 2 .…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species modulator 1 regulates oxidative stress and induces renal and pulmonary fibrosis in a unilateral ureteral obstruction rat model and in HK-2 cells

Liu

Xia

et al. 2017

Molecular Medicine Reports

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Renal interstitial fibrosis (RIF) is the main process that leads to renal failure. It is necessary to investigate the mechanism of RIF and identify appropriate methods of regulating it. Furthermore, unilateral ureteral obstruction is a frequently used model for the study of RIF. The morphological damage associated with kidney and lung dysfunction was detected using histopathological experiments. Subsequently, high expression of reactive oxygen species (ROS) modulator 1 (ROMO1) and ROS was measured in blood serum. In addition, epithelial-mesenchymal transition marker, transforming growth factor β (TGF-β) and mothers against decapentaplegic homolog 2/3 expression was evaluated using the reverse transcription-quantitative polymerase chain reaction and western blotting. All serious symptoms were relieved to a certain extent following oxidation inhibitor intervention using three common antioxidants. HK-2 cells were treated with H2O2 to cause oxidative stress, and ROMO1 and fibrosis marker expression increased; however, activation was suppressed byROMO1 knockout. The present study provides evidence that the expression of ROMO1 induces ROS production and activates the TGF-β signaling pathway. It may be concluded that ROMO1 helps to provide a molecular basis for improved clinical intervention and prognosis of patients.

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Section: Discussionmentioning

confidence: 99%

Reactive oxygen species modulator 1 regulates oxidative stress and induces renal and pulmonary fibrosis in a unilateral ureteral obstruction rat model and in HK-2 cells

Liu

Xia

et al. 2017

Molecular Medicine Reports

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“…The production and migration of the fibers, which are primarily composed of actin and myosin, were also suppressed by H 2 O 2 in a more aggressive breast cancer cell line (MDA‐MB‐231). These results suggest that that proliferation of breast cancer cells is modulated directly by ROS via the modulation gene that encodes for the cellular cycle and apoptosis (112). These two recent findings changed the views of ROS as a deleterious molecule and even assigned it a potential essential role in the diminution of the progression in some cancers ( Fig.…”

Section: Physiological Implications Of Rosmentioning

confidence: 98%

“…Oridonin increased intracellular ROS levels, whereas pretreatment with the ROS scavenger, N ‐acetyl‐ l ‐cysteine, dramatically abrogated RAR‐α stabilization, which indicates the positive role of ROS in oridonin‐induced RAR‐α stabilization (111). In addition, Ma et al (112) observed that ROS production (H 2 O 2 ) inhibits proliferation and induces apoptosis in MCF‐7 breast cancer cells via the modulation of cell cycle and apoptosis‐related genes, and inhibits migration by decreasing stress fibers via DLC1/RhoA signaling. The production and migration of the fibers, which are primarily composed of actin and myosin, were also suppressed by H 2 O 2 in a more aggressive breast cancer cell line (MDA‐MB‐231).…”

Section: Physiological Implications Of Rosmentioning

confidence: 99%

Physiological role of reactive oxygen species as promoters of natural defenses

et al. 2017

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It has been 60 yr since the discovery of reactive oxygen species (ROS) in biology and the beginning of the scientific community's attempt to understand the impact of the unpaired electron of ROS molecules in biological pathways, which was eventually noted to be toxic. Several studies have shown that the presence of ROS is essential in triggering or acting as a secondary factor for numerous pathologies, including metabolic and genetic diseases; however, it was demonstrated that chronic treatment with antioxidants failed to show efficacy and positive effects in the prevention of diseases or health complications that result from oxidative stress. On the contrary, such treatment has been shown to sometimes even worsen the disease. Because of the permanent presence of ROS in organisms, elaborate mechanisms to adapt with these reactive molecules and to use them without necessarily blocking or preventing their actions have been studied. There is now a large body of evidence that shows that living organisms have conformed to the presence of ROS and, in retrospect, have adapted to the bioactive molecules that are generated by ROS on proteins, lipids, and DNA. In addition, ROS have undergone a shift from being molecules that invoked oxidative damage in regulating signaling pathways that impinged on normal physiological and redox responses. Working in this direction, this review unlocks a new conception about the involvement of cellular oxidants in the maintenance of redox homeostasis in redox regulation of normal physiological functions, and an explanation for its essential role in numerous pathophysiological states is noted.-Roy, J., Galano, J.-M., Durand, T., Le Guennec, J.-Y., Lee, J. C.-Y. Physiological role of reactive oxygen species as promoters of natural defenses.

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“…The downregulating effect of superoxide anion and hydrogen peroxide on Cav-1 was mediated through a transcription-independent mechanism that involved protein degradation via the ubiquitin-proteasome pathway [ 63 ]. In H1299, non-small lung cancer cells, 100 μ M of H 2 O 2 inhibited migration, upregulated Deleted in Liver Cancer 1 (DLC1) protein expression, and reduced the activity of RhoA [ 64 ]. Thus, H 2 O 2 may be used as an inhibitor of cancer cell proliferation, migration, and invasion if used at particular concentrations and cancer cell types.…”

Section: Paradoxical Effects Of H 2 O mentioning

confidence: 99%

Molecular and Cellular Effects of Hydrogen Peroxide on Human Lung Cancer Cells: Potential Therapeutic Implications

Vilema-Enríquez

Arroyo

Grijalva

et al. 2016

Oxidative Medicine and Cellular Longevity

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Lung cancer has a very high mortality-to-incidence ratio, representing one of the main causes of cancer mortality worldwide. Therefore, new treatment strategies are urgently needed. Several diseases including lung cancer have been associated with the action of reactive oxygen species (ROS) from which hydrogen peroxide (H2O2) is one of the most studied. Despite the fact that H2O2 may have opposite effects on cell proliferation depending on the concentration and cell type, it triggers several antiproliferative responses. H2O2 produces both nuclear and mitochondrial DNA lesions, increases the expression of cell adhesion molecules, and increases p53 activity and other transcription factors orchestrating cancer cell death. In addition, H2O2 facilitates the endocytosis of oligonucleotides, affects membrane proteins, induces calcium release, and decreases cancer cell migration and invasion. Furthermore, the MAPK pathway and the expression of genes related to inflammation including interleukins, TNF-α, and NF-κB are also affected by H2O2. Herein, we will summarize the main effects of hydrogen peroxide on human lung cancer leading to suggesting it as a potential therapeutic tool to fight this disease. Because of the multimechanistic nature of this molecule, novel therapeutic approaches for lung cancer based on the use of H2O2 may help to decrease the mortality from this malignancy.

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H₂O₂Inhibits Proliferation and Mediates Suppression of Migration via DLC1/RhoA Signaling in Cancer Cells

Cited by 22 publications

References 32 publications

Reactive oxygen species modulator 1 regulates oxidative stress and induces renal and pulmonary fibrosis in a unilateral ureteral obstruction rat model and in HK-2 cells

Reactive oxygen species modulator 1 regulates oxidative stress and induces renal and pulmonary fibrosis in a unilateral ureteral obstruction rat model and in HK-2 cells

Physiological role of reactive oxygen species as promoters of natural defenses

Molecular and Cellular Effects of Hydrogen Peroxide on Human Lung Cancer Cells: Potential Therapeutic Implications

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H2O2Inhibits Proliferation and Mediates Suppression of Migration via DLC1/RhoA Signaling in Cancer Cells

Cited by 22 publications

References 32 publications

Reactive oxygen species modulator 1 regulates oxidative stress and induces renal and pulmonary fibrosis in a unilateral ureteral obstruction rat model and in HK-2 cells

Reactive oxygen species modulator 1 regulates oxidative stress and induces renal and pulmonary fibrosis in a unilateral ureteral obstruction rat model and in HK-2 cells

Physiological role of reactive oxygen species as promoters of natural defenses

Molecular and Cellular Effects of Hydrogen Peroxide on Human Lung Cancer Cells: Potential Therapeutic Implications

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H₂O₂Inhibits Proliferation and Mediates Suppression of Migration via DLC1/RhoA Signaling in Cancer Cells