A Mixture of Chemopreventives Modifying the Oxidative State and Inducing Programmed Cell Death in Human and Hamster Oral Carcinoma Cells

1998 ◽  
Vol 3 (3) ◽  
pp. 175-190
Author(s):  
Joel L. Schwartz
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Carcinoma Cells ◽  
Oral Carcinoma ◽  
Oxidative State

Disruption of SIRT7 Increases the Efficacy of Checkpoint Inhibitor via MEF2D Regulation of Programmed Cell Death 1 Ligand 1 in Hepatocellular Carcinoma Cells

2020 ◽  
Vol 158 (3) ◽  
pp. 664-678.e24 ◽  
Author(s):  
Junyu Xiang ◽  
Ni Zhang ◽  
Hui Sun ◽  
Li Su ◽  
Chengcheng Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Checkpoint Inhibitor ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Programmed Cell Death 1

Amine oxidases, programmed cell death, and tissue renewal

1990 ◽  
Vol 327 (1239) ◽  
pp. 67-74 ◽  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Inner Cell Mass ◽  
Amine Oxidase ◽  
Cell Mass ◽  
Embryoid Bodies ◽  
Carcinoma Cells ◽  
The Other ◽  
Amine Oxidases ◽  
Toxic Activity

Embryonal carcinoma cells, with embryonic (ECaE) or trophectodermal (ECaT) potential, have been used in a colony assay to determine regulatory mechanisms in the blastocyst. The mechnism that regulates ECaE and results in chimera formation is dependent upon a soluble factor in blastocoele fluid and contact with trophectoderm. Two mechanisms contribute to the regulation of ECaT: one involves a factor in blastocoele fluid and the other contact with either trophectoderm or inner cell mass which results in differentiation of the cells into trophectoderm, and the other involves the killing of at least 40% of the cells by blastocoele fluid alone. This cytotoxic activity probably causes the programmed cell death that occurs in the inner cell mass during blastulation as it loses the potential to differentiate into trophectoderm. A toxic activity similar to that of normal blastocysts has been obtained from embryoid bodies. This activity is caused by amine oxidase-dependent catabolism of polyamines, and it is postulated that programmed cell death in the embryo and chalone activity in the adult may have similar mechanisms.

scholarly journals The fate of Krüppel-like factor 9-positive hepatic carcinoma cells may be determined by the programmed cell death protein 5

2013 ◽  
Vol 44 (1) ◽  
pp. 153-160 ◽  
Author(s):  
DA-ZHI FU ◽  
YING CHENG ◽  
HUI HE ◽  
HAI-YANG LIU ◽  
YONG-FENG LIU
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Carcinoma Cells ◽  
Hepatic Carcinoma ◽  
Cell Death Protein

scholarly journals MicroRNA-182 Promotes Cell Migration by Targeting Programmed Cell Death 4 in Hepatocellular Carcinoma Cells

2020 ◽  
Vol Volume 13 ◽  
pp. 9159-9167
Author(s):  
Junwei Hu ◽  
Zeyu Wang ◽  
Jinjun Wang ◽  
Yicheng Jian ◽  
Jiarun Dai ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Cell Migration ◽  
Programmed Cell Death ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Programmed Cell Death 4

CJK-7, a Novel Flavonoid from Paulownia tomentosa Triggers Cell Death Cascades in HCT-116 Human Colon Carcinoma Cells via Redox Signaling

2018 ◽  
Vol 18 (3) ◽  
pp. 428-437 ◽  
Author(s):  
Mahendra Pal Singh ◽  
Ki Hun Park ◽  
Tejinder Pal Khaket ◽  
Sun Chul Kang
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Paulownia Tomentosa ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
Hct 116

Background: Colon cancer is the second most common cancer to cause death worldwide. About half of colon cancers patients require adjuvant therapy to control relapse following surgical resection. Therefore, abolition of tumor cell progression using an effective chemotherapeutic agent holds a feasible approach to treat patients suffering from colon cancer. In the present study, we evaluated the effects of geranylated flavonoid CJK-7, isolated from Paulownia tomentosa on HCT-116 human colon carcinoma cells. Materials and Methods: The effects of CJK-7 as an active component on HCT-116 cells programmed cell death and its underlying molecular mechanism were examined by using MTT assay, morphological assessment, H2DCFDA staining, Fura-2AM staining, Hoechst-33342 staining, comet assay, Acridine orange staining, mitochondrial membrane potential (ΔΨm) assay and Western blot analyses. Results and Conclusion: The results revealed that, CJK-7 was capable of inducing caspase-dependent cell death events in cancer cells. Moreover, it was involved in up-regulation of autophagy signaling as evidenced by enhanced expression of LC3I/II. We also noticed stimulated expression of endoplasmic reticulum stress markers and phosphorylation of c-Jun NH2-terminal kinase (JNK), which was associated with up-regulated expression of p53, PUMA, Atg5 and Beclin-1, and down-regulation of Bcl-2, stressing the interaction of ROS on the aforementioned signaling. Furthermore, exposure to ROS scavengers (N-acetyl-l-cysteine (NAC), and JNK-specific inhibitor SP600125) significantly reversed the effects of CJK-7 by down-regulating apoptosis and autophagy signatures in HCT-116 cancer cells. Collectively our findings clarify the ROS-dependent regulatory effect of CJK-7 on programmed cell death signaling events in HCT-116 cancer cells while depicting its virile pro-oxidant capacity.

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