scholarly journals PCDH9 target RAC1/ROS-NADPH-oxidase complex with the assistance of Pyk2 interaction through Cyclin D1 trafficking

2020 ◽  
Author(s):  
Jiaojiao Zhang ◽  
Hui-Zhi Yang ◽  
Shuang Liu ◽  
Md Obaidul Islam ◽  
Yue Zhu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Migration ◽  
Malignant Melanoma ◽  
Nadph Oxidase ◽  
Cell Viability ◽  
Cyclin D1 ◽  
Normal Skin ◽  
Melanoma Cells ◽  
Melanoma Progression ◽  
Nadph Oxidase Complex

Abstract Background: Melanoma has dramatically increased during last 30 years with low five-year survival and prognosis rate.Methods: Melanoma cells (A375 and G361) were chosen as in vitro model. The interference and overexpression of PCDH9 were infected by lentivirus. The effects of PCDH9 on melanoma cells were assessed in terms of alteration of PCDH9 such as cell viability, apoptosis, cell cycle and wound-healing assay. Moreover, expressions of PCDH9 with other genes (MMP2, MMP9, Pyk2 Cyclin D1, RAC1 and FAK) were also assessed by PCR and western blotting, immunohistochemical analysis. The protein complex immunoprecipitation was operated for protein-protein interaction (PPI) of PCDH9. Originlab 2020 was used for statistical analysis.Results: Melanoma cells treated with PCDH9 showed influence melanoma as similar function as Hace1 that regulate RAC1/ROS-dependent NADPH oxidase complexes through targeting complex-bound RAC1 with the help of Pyk2, while RAC1 directly influence RAC1/ROS-NADPH-oxidase complex to induce metalloproteinases (MMPs), that are involved in cell migration and proliferation. Moreover, PCDH9 could influence the expressions of MMP2, MMP9, Pyk2, Cyclin D1 and RAC1, except FAK, decreased cell viability, cell migration and increased apoptosis, but did not exert significant effects on cell cycle. Besides, the immunohistochemical results exhibited lower PCDH9 expression in malignant melanoma samples than benign naevus tissue or/and normal skin, and PCDH9 was expressed in the cytoplasm rather than nuclei. The results of immunoprecipitation demonstrated that PCDH9 bind with RAC1 and Pyk2, suggesting the regulation of PCDH9 to melanoma progression. Conclusion: Our results suggest that PCDH9 and RAC1 could predict for potential biomarkers prognosis of malignant melanoma, interestingly, with Pyk2’s assistance like a bridge PCDH9 can modulate melanoma progression by interacting with RAC1.

scholarly journals Tumour Progression Stage-Dependent Secretion of YB-1 Stimulates Melanoma Cell Migration and Invasion

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2328 ◽  
Author(s):  
Corinna Kosnopfel ◽  
Tobias Sinnberg ◽  
Birgit Sauer ◽  
Heike Niessner ◽  
Alina Muenchow ◽  
...  
Keyword(s):  
Cell Migration ◽  
Malignant Melanoma ◽  
Melanoma Cell ◽  
Cell Biology ◽  
Secretory Pathway ◽  
Tumour Progression ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Melanoma Progression ◽  
And Migration

Secreted factors play an important role in intercellular communication. Therefore, they are not only indispensable for the regulation of various physiological processes but can also decisively advance the development and progression of tumours. In the context of inflammatory disease, Y-box binding protein 1 (YB-1) is actively secreted and the extracellular protein promotes cell proliferation and migration. In malignant melanoma, intracellular YB-1 expression increases during melanoma progression and represents an unfavourable prognostic marker. Here, we show active secretion of YB-1 from melanoma cells as opposed to benign cells of the skin. Intriguingly, YB-1 secretion correlates with the stage of melanoma progression and depends on a calcium- and ATP-dependent non-classical secretory pathway leading to the occurrence of YB-1 in the extracellular space as a free protein. Along with an elevated YB-1 secretion of melanoma cells in the metastatic growth phase, extracellular YB-1 exerts a stimulating effect on melanoma cell migration, invasion, and tumourigenicity. Collectively, these data suggest that secreted YB-1 plays a functional role in melanoma cell biology, stimulating metastasis, and may serve as a novel biomarker in malignant melanoma that reflects tumour aggressiveness.

scholarly journals Antioxidative and Antimelanoma Effects of Various Tea Extracts via a Green Extraction Method

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Yihui Chen ◽  
Jyun-Yin Huang ◽  
Yichi Lin ◽  
I-Fan Lin ◽  
Yi-Ru Lu ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Cell Viability ◽  
Green Tea ◽  
Metal Ion ◽  
Normal Skin ◽  
Reducing Power ◽  
Black Tea ◽  
Melanoma Cells ◽  
Human Malignant Melanoma ◽  
Oolong Tea

Tea (Camellia sinensis) contains high level of antioxidant elements and is a well-known beverage consumed worldwide. The purpose of this study is to compare different concentrations of green tea, black tea, oolong tea 861, oolong tea 732, and jasmine green tea. These five types of tea extracts were known to have antioxidative properties, reducing power, and metal ion chelating activity. The current study compared these five extracts in terms of their inhibiting effects on human malignant melanoma: A2058 and A375. To determine the cell viability between normal cell and malignant melanoma cells, an MTT assay was applied to evaluate the cytotoxic potential on human melanoma cells, with all tea extracts showing decreased cell viability with increasing tea extract concentrations. Cytotoxicity on HaCat (normal skin cells) showed no effect on the cell viabilities at lower concentrations of the tea extracts. These results suggest the antioxidative effect of five tea extracts that protect against oxidation and melanoma production, with green tea and jasmine green tea showing the lowest cell viability when tested against malignant melanoma cells.

MicroRNA-143-3p inhibits growth and invasiveness of melanoma cells by targeting cyclooxygenase-2 and inversely correlates with malignant melanoma progression

2018 ◽  
Vol 156 ◽  
pp. 52-59 ◽  
Author(s):  
Elisabetta Panza ◽  
Giuseppe Ercolano ◽  
Paola De Cicco ◽  
Chiara Armogida ◽  
Giosuè Scognamiglio ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Melanoma Cells ◽  
Cyclooxygenase 2 ◽  
Melanoma Progression

scholarly journals Ticagrelor and clopidogrel suppress NF-κB to treat acute coronary syndrome

2019 ◽  
Author(s):  
Zhuyin Jia ◽  
Yiwei Huang ◽  
Xiaojun Ji ◽  
Jiaju Sun ◽  
Guosheng Fu
Keyword(s):  
Cell Cycle ◽  
Acute Coronary Syndrome ◽  
Cell Migration ◽  
Cell Viability ◽  
Umbilical Vein ◽  
Quantitative Polymerase Chain Reaction ◽  
Statistical Significance ◽  
Inflammatory Factors ◽  
Mrna Levels ◽  
Coronary Syndrome

Abstract Background: Inflammatory cytokines are involved in acute coronary syndrome (ACS),and NF-kB is the central regulator of inflammation. Moreover, ticagrelor and clopidogrelcan prevent thrombotic events and improve the care of patients with ACS. Thus, we speculated that ticagrelor and clopidogrel relieve ACS by regulating NF-kB pathway. Methods: After human umbilical vein endothelial cells (HUVECs) were cultured with ticagrelor or clopidogrel and given lipopolysaccharide (LPS) and CD14, the mRNA levels of related inflammatory factors, the protein level changes of molecules in the NF-kB pathway, and the changes in cell viability, apoptosis and the cell cycle, cell migration, vascular formation and other vital activities were detected using quantitative Polymerase chain reaction (qPCR), Western blotting and immunofluorescence assay, CCK8， flow cytometry, transwell assay, matrigel, respectively. All data was expressed as the mean ± S.D. The statistical significance of data was assessedby an unpaired two-tailed t-test. Results: Ticagrelor and clopidogrel can suppress the NF-kB pathway by inhibiting the phosphorylation and entry into the nucleus of p65, restraining the degradation of IKBa, improving cell viability, restoring the cell cycle, cell migration and angiogenic ability, and inhibiting apoptosis. Conclusions: Ticagrelor and clopidogrel alleviate cellular dysfunction through suppressing NF-kB signaling to treat acute coronary syndrome.

scholarly journals Beta3-Tubulin Is Critical for Microtubule Dynamics, Cell Cycle Regulation, and Spontaneous Release of Microvesicles in Human Malignant Melanoma Cells (A375)

2020 ◽  
Vol 21 (5) ◽  
pp. 1656
Author(s):  
Mohammed O. Altonsy ◽  
Anutosh Ganguly ◽  
Matthias Amrein ◽  
Philip Surmanowicz ◽  
Shu Shun Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Malignant Melanoma ◽  
Structural Changes ◽  
Melanoma Cells ◽  
Neoplastic Cell ◽  
Primary Component ◽  
Cellular Growth ◽  
Class Iii ◽  
M Cell ◽  
Human Malignant Melanoma

Microtubules (MTs), microfilaments, and intermediate filaments, the main constituents of the cytoskeleton, undergo continuous structural changes (metamorphosis), which are central to cellular growth, division, and release of microvesicles (MVs). Altered MTs dynamics, uncontrolled proliferation, and increased production of MVs are hallmarks of carcinogenesis. Class III beta-tubulin (β3-tubulin), one of seven β-tubulin isotypes, is a primary component of MT, which correlates with enhanced neoplastic cell survival, metastasis and resistance to chemotherapy. We studied the effects of β3-tubulin gene silencing on MTs dynamics, cell cycle, and MVs release in human malignant melanoma cells (A375). The knockdown of β3-tubulin induced G2/M cell cycle arrest, impaired MTs dynamics, and reduced spontaneous MVs release. Additional studies are therefore required to elucidate the pathophysiologic and therapeutic role of β3-tubulin in melanoma.

scholarly journals Overexpression of Ras-Related C3 Botulinum Toxin Substrate 2 Radiosensitizes Melanoma Cells In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Wentao Hu ◽  
Lin Zhu ◽  
Weiwei Pei ◽  
Shuxian Pan ◽  
Ziyang Guo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Botulinum Toxin ◽  
Malignant Melanoma ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Melanoma Cells ◽  
Oxygen Species ◽  
X Rays ◽  
Nadph Oxidase Activity ◽  
Carbon Ion

Radioresistance is the major obstacle in the radiotherapy of the malignant melanoma. Thus, it is of importance to increase the radiosensitivity of melanoma cells. In the present study, the radioresistant melanoma cell line OCM-1 with inducible overexpression of Ras-related C3 botulinum toxin substrate 2 was established based on a radiation-inducible early growth response gene (Egr-1) promoter. The effects of Ras-related C3 botulinum toxin substrate 2 overexpression on the radiosensitivity of melanoma cells exposed to either X-rays or carbon ion beams were evaluated in cultured cells as well as xenograft tumor models. In addition, both reactive oxygen species yield and the NADPH oxidase activity were measured in the irradiated melanoma cells. It was found that the radiation-inducible overexpression of Ras-related C3 botulinum toxin substrate 2 sensitized the melanoma cells to both X-rays and carbon ion irradiation by enhancing the NADPH oxidase activity and the subsequent reactive oxygen species production. Besides, the overexpression of Ras-related C3 botulinum toxin substrate 2 enhanced the tumor-killing effect of radiotherapy in xenograft tumors significantly. The results of this study indicate that Ras-related C3 botulinum toxin substrate 2 is promising in increasing the radiosensitivity of melanoma cells, which provides experimental evidence and theoretical basis for clinical radiosensitization of the malignant melanoma.

Resveratrol induces cell cycle arrest and apoptosis in epithelioid malignant pleural mesothelioma cells

2017 ◽  
Vol 43 (2) ◽  
pp. 197-204
Author(s):  
Saime Batirel ◽  
Ergul Mutlu Altundag ◽  
Selina Toplayici ◽  
Ceyda Corek ◽  
Hasan Fevzi Batirel
Keyword(s):  
Cell Cycle ◽  
Cell Viability ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Malignant Pleural Mesothelioma ◽  
Cell Cycle Distribution ◽  
Pleural Mesothelioma ◽  
Dependent Manner ◽  
P53 Expression ◽  
Cycle Arrest

Abstract Background: Resveratrol is a natural anti-carcinogenic polyphenol. Malignant pleural mesothelioma (MPM) is an aggressive tumor with poor prognosis. In this study, we investigated the effects of resveratrol on epithelioid MPM. Material and methods: Human epithelioid MPM cell line (NCI-H2452) was exposed to resveratrol (5–200 μM) for 24 or 48 h. Cell viability was assessed by WST-1 assay. Flow cytometry analyses were performed to evaluate the effects of resveratrol on cell cycle distribution and apoptosis. Western blot analysis was used to determine protein expression levels of antioxidant enzymes, cyclin D1 and p53. Reactive oxygen species (ROS) were measured using H2DCFDA. Results: Resveratrol reduced cell viability of the cells in a concentration and time dependent manner. After treatment, the cells accumulated in G0/G1 phase and the percentage of cells in G2/M phase was reduced. Resveratrol decreased cyclin D1 and increased p53 expression in cell lysates. Treated cells exhibited increased apoptotic activity. ROS were elevated with resveratrol treatment, but there was no change in the expression of superoxide dismutase (SOD)-1, SOD-2 and glutathione peroxidase. Conclusion: Our results revealed that resveratrol exhibits anti-cell viability effect on epithelioid MPM cells by inducing cell cycle arrest and apoptosis. Resveratrol may become a potential therapeutic agent for epithelioid MPM.

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