scholarly journals Mesoporous silica particles functionalized with newly extracted fish oil (Omeg@Silica) inhibit lung cancer cell growth

Nanomedicine ◽  
2021 ◽  
Vol 16 (23) ◽  
pp. 2061-2074
Author(s):  
Caterina Di Sano ◽  
Claudia D’Anna ◽  
Antonino Scurria ◽  
Claudia Lino ◽  
Mario Pagliaro ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Mesoporous Silica ◽  
Fish Oil ◽  
Cancer Cells ◽  
Oxygen Species ◽  
Lung Cancer Cell ◽  
Antitumor Effects ◽  
Silica Microparticles

Aim: To assess whether Omeg@Silica microparticles – fish oil from anchovy fillet leftovers (AnchoisOil) encapsulated within mesoporous silica particles – are effective in promoting antitumor effects in lung cancer cells. Methods: Three human non-small-cell lung cancer cell lines (A549, Colo 699 and SK-MES-1) were used. Cells were treated with AnchoisOil dispersed in ethanol (10 and 15 μg/ml) or encapsulated in silica and further formulated in aqueous ethanol. Cell cycle, reactive oxygen species, mitochondrial stress and long-term proliferation were assessed. Results & conclusion: Omeg@Silica microparticles were more effective than fish oil in increasing reactive oxygen species and mitochondrial damage, and in altering the cell cycle and reducing cell proliferation, in lung cancer cells. These in vitro antitumor effects of Omeg@Silica support its investigation in lung cancer therapy.

scholarly journals Mesoporous silica particles functionalized with newly extracted fish oil (Omeg@Silica) inhibit lung cancer cell growth

2021 ◽  
Author(s):  
Caterina Di Sano ◽  
Claudia D’Anna ◽  
Antonino Scurria ◽  
Claudia Lino ◽  
Mario Pagliaro ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Mesoporous Silica ◽  
Fish Oil ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Nsclc Cell ◽  
Lung Cancer Cell ◽  
Antitumor Effects

AbstractOmeg@Silica microparticles consisting of whole fish oil rich in omega-3 lipids, vitamin D3 and zeaxanthin extracted with biobased limonene from anchovy fillet leftovers (AnchoisOil) encapsulated within mesoporous silica particles are highly effective in modulating oxidative stress, mitochondrial damage or in promoting antitumor effects in lung cancer cells. A panel of three different human non-small cell lung cancer (NSCLC) cell lines (A549, Colo 699 and SKMES) was used. Cancer cells were treated with AnchoisOil dispersed in ethanol (10 and 15 μg/ml) or encapsulated in silica, and cell cycle, reactive oxigen species (ROS) and mitochondrial stress (MitoSOX) assessed by flow cytometry. The effects on long-term proliferation (clonogenic assay) were also evaluated. The sub-micron Omeg@Silica microparticles were more effective than fish oil alone in increasing ROS and mitocondrial damage, in altering cell cycle as well as in reducing colony formation ability in the tested lung cancer cell lines. These results suggest that Omeg@Silica mesoporous silica functionalized with whole fish oil has antitumor effects in NSCLC cell lines and support its investigation in lung cancer therapy.

MG132 as a proteasome inhibitor induces cell growth inhibition and cell death in A549 lung cancer cells via influencing reactive oxygen species and GSH level

2010 ◽  
Vol 29 (7) ◽  
pp. 607-614 ◽  
Author(s):  
Yong Hwan Han ◽  
Woo Hyun Park
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Cell Death ◽  
Cancer Cells ◽  
Proteasome Inhibitor ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Oxygen Species ◽  
A549 Lung

Carbobenzoxy-Leu-Leu-leucinal (MG132) as a proteasome inhibitor has been shown to induce apoptotic cell death through formation of reactive oxygen species (ROS). In the present study, we evaluated the effects of MG132 on the growth of A549 lung cancer cells in relation to cell growth, ROS and glutathione (GSH) levels. Treatment with MG132 inhibited the growth of A549 cells with an IC50 of approximately 20 μM at 24 hours. DNA flow cytometric analysis indicated that 0.5 ∼ 30 μM MG132 induced a G1 phase arrest of the cell cycle in A549 cells. Treatment with 10 or 30 μM MG132 also induced apoptosis, as evidenced by sub-G1 cells and annexin V staining cells. This was accompanied by the loss of mitochondrial membrane potential (MMP; Δψm). The intracellular ROS levels including O2•- were strongly increased in 10 or 30 μM MG132-treated A549 cells but were down-regulated in 0.1, 0.5 or 1 μM MG132-treated cells. Furthermore, 10 or 30 μM MG132 increased mitochondrial O2•- level but 0.1, 0.5 or 1 μM MG132 decreased that. In addition, 10 or 30 μM MG132 induced GSH depletion in A549 cells. In conclusion, MG132 inhibited the growth of human A549 cells via inducing the cell cycle arrest as well as triggering apoptosis, which was in part correlated with the changes of ROS and GSH levels. Our present data provide important information on the anti-growth mechanisms of MG132 in A549 lung cancer cells in relation to ROS and GSH.

Effect of zoledronic acid combined with cisplatin and paclitaxel on inhibition of non-small cell lung cancer cell lines

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e19095-e19095
Author(s):  
Z. Gao ◽  
B. Han ◽  
J. Teng
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Zoledronic Acid ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cell ◽  
Antitumor Effects

e19095 Backgrounds: Recent studies reported that zoledronic acid, a biphosphonate with proposed apoptotic activity, could cause a direct antitumor effect. Our prior study [J Clin Oncol 26: 2008 (May 20 suppl; abstr 19116)] reported that Zoledronic acid combined with Cisplatin shows significantly synergistic antitumor effects on lung cancer cell line A549 and subcutaneous implanted tumor on nude mice. Investigate whether zoledronic acid, augmented the cytotoxicity of cisplatin and/or paclitaxel in A549 lung cancer cell line. Methods: This cell line was subjected to different concentrations of the above chemotherapeutic agents and zoledronic acid. Cytotoxicity was assessed by the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrasodium bromide) assay. Flow cytometry was used to examine cell cycle,cell apoptosis rate. Results: Zoledronic acid in in 50 micromolar (mM) concentration augmented the cytotoxicity by cisplatin in 10μmol/L and paclitaxel in 5μmol/L. Zoledronic acid could inhibit the proliferation of lung cancer cells in vitro,which was associated with arresting of G1 phase and inducing apoptosis by a time-dependent and dose-dependentmanner. The apoptosis rate of cell increased after zoledronic acid combined with cisplatin and/or paclitaxel. Conclusions: Zoledronic acid can induce apoptosis and block cell cycle of lung cancer cells. Zoledronic acid has also shown synergistic antitumor effects when combined with cisplatin and/or paclitaxel. The clinical potential of this finding should be further studied. No significant financial relationships to disclose.

Reserpine Induces Apoptosis and Cell Cycle Arrest in Hormone Independent Prostate Cancer Cells through Mitochondrial Membrane Potential Failure

2019 ◽  
Vol 18 (9) ◽  
pp. 1313-1322 ◽  
Author(s):  
Manjula Devi Ramamoorthy ◽  
Ashok Kumar ◽  
Mahesh Ayyavu ◽  
Kannan Narayanan Dhiraviam
Keyword(s):  
Prostate Cancer ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Prostate Cancer Cells

Background: Reserpine, an indole alkaloid commonly used for hypertension, is found in the roots of Rauwolfia serpentina. Although the root extract has been used for the treatment of cancer, the molecular mechanism of its anti-cancer activity on hormonal independent prostate cancer remains elusive. Methods: we evaluated the cytotoxicity of reserpine and other indole alkaloids, yohimbine and ajmaline on Prostate Cancer cells (PC3) using MTT assay. We investigated the mechanism of apoptosis using a combination of techniques including acridine orange/ethidium bromide staining, high content imaging of Annexin V-FITC staining, flow cytometric quantification of the mitochondrial membrane potential and Reactive Oxygen Species (ROS) and cell cycle analysis. Results: Our results indicate that reserpine inhibits DNA synthesis by arresting the cells at the G2 phase and showed all standard sequential features of apoptosis including, destabilization of mitochondrial membrane potential, reduced production of reactive oxygen species and DNA ladder formation. Our in silico analysis further confirmed that indeed reserpine docks to the catalytic cleft of anti-apoptotic proteins substantiating our results. Conclusion: Collectively, our findings suggest that reserpine can be a novel therapeutic agent for the treatment of androgen-independent prostate cancer.

scholarly journals Mitochondria-Targeted Antioxidants MitoQ and MitoTEMPO Do Not Influence BRAF-Driven Malignant Melanoma and KRAS-Driven Lung Cancer Progression in Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 163
Author(s):  
Kristell Le Gal ◽  
Clotilde Wiel ◽  
Mohamed X. Ibrahim ◽  
Marcus Henricsson ◽  
Volkan I. Sayin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Malignant Melanoma ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Nuclear Dna ◽  
Human Melanoma ◽  
Oxygen Species ◽  
Lung Cancer Cell ◽  
Primary Tumors ◽  
Anti Cancer

Cancer cells produce high levels of mitochondria-associated reactive oxygen species (ROS) that can damage macromolecules, but also promote cell signaling and proliferation. Therefore, mitochondria-targeted antioxidants have been suggested to be useful in anti-cancer therapy, but no studies have convincingly addressed this question. Here, we administered the mitochondria-targeted antioxidants MitoQ and MitoTEMPO to mice with BRAF-induced malignant melanoma and KRAS-induced lung cancer, and found that these compounds had no impact on the number of primary tumors and metastases; and did not influence mitochondrial and nuclear DNA damage levels. Moreover, MitoQ and MitoTEMPO did not influence proliferation of human melanoma and lung cancer cell lines. MitoQ and its control substance dTPP, but not MitoTEMPO, increased glycolytic rates and reduced respiration in melanoma cells; whereas only dTPP produced this effect in lung cancer cells. Our results do not support the use of mitochondria-targeted antioxidants for anti-cancer monotherapy, at least not in malignant melanoma and lung cancer.

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