Cucurbitacin B induces G2
 arrest and apoptosis via
 a reactive oxygen species-dependent mechanism in human colon adenocarcinoma SW480 cells

Manganese (Mn) oxidation is performed through oxidative Mn-oxidizing bacteria (MnOxb) as the main bio-weathering mechanism for Mn(III/IV) deposits during soil formation. However, with an increase in temperature, the respiration rate also increases, producing Reactive Oxygen Species (ROS) as by-products, which are harmful to microbial cells. We hypothesize that bacterial ROS oxidize Mn(II) to Mn(III/IV) as a secondary non-enzymatic temperature-dependent mechanism for cell protection. Fourteen MnOxb were isolated from Antarctic soils under the global warming effect, and peroxidase (PO) activity, ROS, and Mn(III/IV) production were evaluated for 120 h of incubation at 4 °C, 15 °C, and 30 °C. ROS contributions to Mn oxidation were evaluated in Arthrobacter oxydans under antioxidant (Trolox) and ROS-stimulated (menadione) conditions. The Mn(III/IV) concentration increased with temperature and positively correlated with ROS production. ROS scavenging with Trolox depleted the Mn oxidation, and ROS-stimulant increased the Mn precipitation in A. oxydans. Increasing the Mn(II) concentration caused a reduction in the membrane potential and bacterial viability, which resulted in Mn precipitation on the bacteria surface. In conclusion, bacterial ROS production serves as a complementary non-enzymatic temperature-dependent mechanism for Mn(II) oxidation as a response in warming environments.

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Author Correction: FTY720 Induces Autophagy-Associated Apoptosis in Human Oral Squamous Carcinoma Cells, in Part, through a Reactive Oxygen Species/Mcl-1-Dependent Mechanism

Scientific Reports ◽

10.1038/s41598-020-60297-8 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Li-Yuan Bai ◽

Chang-Fang Chiu ◽

Shih-Jiuan Chiu ◽

Po-Chen Chu ◽

Jing-Ru Weng

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Squamous Carcinoma ◽

Carcinoma Cells ◽

Oxygen Species ◽

Squamous Carcinoma Cells ◽

Oral Squamous Carcinoma ◽

Dependent Mechanism

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2019-0131 ◽

2019 ◽

Vol 97 (12) ◽

pp. 1176-1184 ◽

Cited By ~ 3

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.

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