Reactive Oxygen Species Act at both TGF-β-Dependent and -Independent Steps during Induction of Apoptosis of Transformed Cells by Normal Cells

1996 ◽  
Vol 222 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Christiane Langer ◽  
Juliane M. Jürgensmeier ◽  
Georg Bauer
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Transformed Cells ◽  
Oxygen Species ◽  
Normal Cells ◽  
Induction Of Apoptosis

scholarly journals Suppression of Reactive Oxygen Species and Enhanced Stress Tolerance in Rubia cordifolia Cells Expressing the rolC Oncogene

2008 ◽  
Vol 21 (12) ◽  
pp. 1561-1570 ◽  
Author(s):  
Victor P. Bulgakov ◽  
Dmitry L. Aminin ◽  
Yuri N. Shkryl ◽  
Tatiana Y. Gorpenchenko ◽  
Galina N. Veremeichik ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Light Stress ◽  
Reactive Oxygen ◽  
Transformed Cells ◽  
Oxygen Species ◽  
Normal Cells ◽  
Rolc Gene ◽  
Rubia Cordifolia ◽  
Cell Assays ◽  
Steady State Levels

It is known that expression of the Agrobacterium rhizogenes rolC gene in transformed plant cells causes defense-like reactions, such as increased phytoalexin production and expression of pathogenesis-related proteins. In the present study, we examined whether this phenomenon is associated with increased production of reactive oxygen species (ROS). Single-cell assays based on confocal microscopy and fluorogenic dyes (2,7-dichlorofluorescein diacetate and dihydrorhodamine 123) showed reduced steady-state levels of ROS in rolC-expressing Rubia cordifolia cells as compared with normal cells. Paraquat, a ROS inducer, caused significant ROS elevation in normal cells but had little effect on rolC-transformed cells. Likewise, ROS elevation triggered by a light stress was suppressed in transformed cells. Our results indicate that the rolC gene acts as a ROS suppressor in unstressed cells and its expression prevents stress-induced ROS elevations. We detected a two- to threefold increase in tolerance of rolC-transformed cells to salt, heat, and cold treatments. Simultaneously, rolC-transformed cells maintained permanently active defensive status, as found by measuring isochorismate synthase gene expression and anthraquinone production. Thus, the oncogene provoked multiple effects in which ROS production and phytoalexin production were clearly dissociated.

scholarly journals Selective induction of apoptosis by capsaicin in transformed cells: the role of reactive oxygen species and calcium

1999 ◽  
Vol 6 (2) ◽  
pp. 155-165 ◽  
Author(s):  
Antonio Macho ◽  
Marco A Calzado ◽  
Juan Muñoz-Blanco ◽  
Consuelo Gómez-Díaz ◽  
Consuelo Gajate ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Transformed Cells ◽  
Oxygen Species ◽  
Induction Of Apoptosis

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

Role of reactive oxygen species in the induction of apoptosis by ?-tocopheryl succinate

2004 ◽  
Vol 112 (3) ◽  
pp. 385-392 ◽  
Author(s):  
Young-Hwa Kang ◽  
Eunmyong Lee ◽  
Moon-Kyung Choi ◽  
Ja-Lok Ku ◽  
So Hee Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tocopheryl Succinate ◽  
Induction Of Apoptosis

scholarly journals Overproduction of reactive oxygen species – obligatory or not for induction of apoptosis by anticancer drugs

2016 ◽  
Vol 28 (4) ◽  
pp. 383-396 ◽  
Author(s):  
Donika Ivanova ◽  
◽  
Zhivko Zhelev ◽  
Ichio Aoki ◽  
Rumiana Bakalova ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Anticancer Drugs ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Induction Of Apoptosis

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.

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