Impressive Suppression of Colon Cancer Growth by Triple Combination SN38/EF24/Melatonin: “Oncogenic” Versus “Onco-Suppressive” Reactive Oxygen Species

2017 ◽  
Vol 37 (10) ◽  
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Reactive Oxygen ◽  
Cancer Growth ◽  
Oxygen Species ◽  
Triple Combination

scholarly journals Ethanol extract of Chrysanthemum zawadskii Herbich induces autophagy and apoptosis in mouse colon cancer cells through the regulation of reactive oxygen species

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Kwang-Youn Kim ◽  
Tae-Woo Oh ◽  
Hye-Jin Yang ◽  
Young-Woo Kim ◽  
Jin-Yeul Ma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Ethanol Extract ◽  
Oxygen Species ◽  
Colon Cancer Cells ◽  
Mouse Colon ◽  
Induced Apoptosis ◽  
Chrysanthemum Zawadskii

Abstract Background Recent research has suggested that autophagy can provide a better mechanism for inducing cell death than current therapeutic strategies. This study investigated the effects of using an ethanol extract of Chrysanthemum zawadskii Herbich (ECZ) to induce apoptosis and autophagy associated with reliable signal pathways in mouse colon cancer CT-26 cells. Methods Using ECZ on mouse colon cancer CT-26 cells, cell viability, annexin V/propidium iodide staining, acridine orange staining, reactive oxygen species (ROS) and western blotting were assayed. Results ECZ exhibited cytotoxicity in CT-26 cells in a dose-dependent manner. ECZ induced apoptosis was confirmed by caspase-3 activation, poly (ADP-ribose) polymerase cleavage, and increased production of reactive oxygen species (ROS). Furthermore, it was shown that ECZ induced autophagy via the increased conversion of microtubule-associated protein 1 light chain 3II, the degradation of p62, and the formation of acidic vesicular organelles. The inhibition of ROS production by N-Acetyl-L-cysteine resulted in reduced ECZ-induced apoptosis and autophagy. Furthermore, the inhibition of autophagy by 3-methyladenine resulted in enhanced ECZ-induced apoptosis via increased ROS generation. Conclusion These findings confirmed that ECZ induced ROS-mediated autophagy and apoptosis in colon cancer cells. Therefore, ECZ may serve as a novel potential chemotherapeutic candidate for colon cancer.

scholarly journals Novel Anthraquinone Compounds Inhibit Colon Cancer Cell Proliferation via the Reactive Oxygen Species/JNK Pathway

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1672 ◽  
Author(s):  
Yuying Li ◽  
Fang Guo ◽  
Yingying Guan ◽  
Tinggui Chen ◽  
Kaiqing Ma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cancer Cell ◽  
Human Cancer ◽  
Hct116 Cell ◽  
Cell Activity ◽  
Similarity Index ◽  
Reactive Oxygen ◽  
Field Analysis ◽  
Oxygen Species

A series of amide anthraquinone derivatives, an important component of some traditional Chinese medicines, were structurally modified and the resulting antitumor activities were evaluated. The compounds showed potent anti-proliferative activities against eight human cancer cell lines, with no noticeable cytotoxicity towards normal cells. Among the candidate compounds, 1-nitro-2-acyl anthraquinone-leucine (8a) showed the greatest inhibition of HCT116 cell activity with an IC50 of 17.80 μg/mL. In addition, a correlation model was established in a three-dimensional quantitative structure-activity relationship (3D-QSAR) study using Comparative Molecular Field Analysis (CoMFA) and comparative molecular similarity index analysis (CoMSIA). Moreover, compound 8a effectively killed tumor cells by reactive oxygen species (ROS)-JNK activation, causing an increase in ROS levels, JNK phosphorylation, and mitochondrial stress. Cytochrome c was then released into cytoplasm, which, in turn activated the cysteine protease pathway and ultimately induced tumor cell apoptosis, suggesting a potential use of this compound for colon cancer treatment.

scholarly journals 3-Bromopyruvate potentiates TRAIL-induced apoptosis in human colon cancer cells through a reactive oxygen species- and caspase-dependent mitochondrial pathway

2019 ◽  
Vol 97 (12) ◽  
pp. 1176-1184 ◽  
Author(s):  
Hassan Abbaszadeh ◽  
Armita Valizadeh ◽  
Masoud Mahdavinia ◽  
Ali Teimoori ◽  
Mohammad Hassan Pipelzadeh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Human Colon ◽  
Inhibitory Effect ◽  
Oxygen Species ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Normal Cells

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a promising anticancer cytokine with minimal toxicity towards normal cells. Nevertheless, most primary cancers are often intrinsically TRAIL-resistant or can acquire resistance after TRAIL therapy. This study aimed to investigate the inhibitory effect of co-treatment of 3-bromopyruvate (3-BP) as a potent anticancer agent with TRAIL on colon cancer cells (HT-29). The results of present study indicated that combined treatment with 3-BP and TRAIL inhibited the proliferation of HT-29 cells to a greater extent (88.4%) compared with 3-BP (54%) or TRAIL (11%) treatment alone. In contrast, the combination of 3-BP and TRAIL had no significant inhibitory effect on the proliferation of normal cells (HEK-293) (8.4%). At a cellular mechanistic level, the present study showed that 3-BP sensitized human colon cancer cells to TRAIL-induced apoptosis via reactive oxygen species generation, upregulation of Bax, downregulation of Bcl-2 and survivin, release of cytochrome c into the cytosol, and activation of caspase-3. In normal cells, 3-BP, TRAIL, or combination of both had no significant effect on the reactive oxygen species levels, release of cytochrome c, and caspase-3 activity. Therefore, the combination of 3-BP and TRAIL can be a promising therapeutic strategy for treatment of colon cancer.

Tu1829 The Effects of Ursodeoxycholic Acid on Cell Cycle, Reactive Oxygen Species, and Proliferation of Colon Cancer Cell

2016 ◽  
Vol 150 (4) ◽  
pp. S955
Author(s):  
Su Young Kim ◽  
Eun-Kyoung Kim ◽  
A Reum Jeong ◽  
Yoon Jae Kim ◽  
Eui Joo Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Ursodeoxycholic Acid ◽  
Cancer Cell ◽  
Reactive Oxygen ◽  
Colon Cancer Cell ◽  
Oxygen Species

scholarly journals Anticancer effect of icaritin inhibits cell growth of colon cancer through reactive oxygen species, Bcl-2 and cyclin D1/E signaling

2016 ◽  
Vol 12 (5) ◽  
pp. 3537-3542 ◽  
Author(s):  
Chaofeng Li ◽  
Weichao Peng ◽  
Xin Song ◽  
Qian Wang ◽  
Wenyue Wang
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cell Growth ◽  
Cyclin D1 ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Anticancer Effect

scholarly journals Protocatechuic Acid, a Simple Plant Secondary Metabolite, Induced Apoptosis by Promoting Oxidative Stress through HO-1 Downregulation and p21 Upregulation in Colon Cancer Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1485
Author(s):  
Rosaria Acquaviva ◽  
Barbara Tomasello ◽  
Claudia Di Giacomo ◽  
Rosa Santangelo ◽  
Alfonsina La Mantia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Protocatechuic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Colon Cancer Cells ◽  
Glutamylcysteine Synthetase

Gastrointestinal cancers, particularly colorectal cancer, are mainly influenced by the dietary factor. A diet rich in fruits and vegetables can help to reduce the incidence of colorectal cancer thanks to the phenolic compounds, which possess antimutagenic and anticarcinogenic properties. Polyphenols, alongside their well-known antioxidant properties, also show a pro-oxidative potential, which makes it possible to sensitize tumor cells to oxidative stress. HO-1 combined with antioxidant activity, when overexpressed in cancer cells, is involved in tumor progression, and its inhibition is considered a feasible therapeutic strategy in cancer treatment. In this study, the effects of protocatechuic acid (PCA) on the viability of colon cancer cells (CaCo-2), annexin V, LDH release, reactive oxygen species levels, total thiol content, HO-1, γ-glutamylcysteine synthetase, and p21 expression were evaluated. PCA induced, in a dose-dependent manner, a significantly reduced cell viability of CaCo-2 by oxidative/antioxidant imbalance. The phenolic acid induced modifications in levels of HO-1, non-proteic thiol groups, γ-glutamylcysteine synthetase, reactive oxygen species, and p21. PCA induced a pro-oxidant effect in cancer cells, and the in vitro pro-apoptotic effect on CaCo-2 cells is mediated by the modulation of redox balance and the inhibition of the HO-1 system that led to the activation of p21. Our results suggest that PCA may represent a useful tool in prevention and/or therapy of colon cancer.

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