scholarly journals Interleukin-4 and interleukin-13 increase NADPH oxidase 1-related proliferation of human colon cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (24) ◽  
pp. 38113-38135 ◽  
Author(s):  
Han Liu ◽  
Smitha Antony ◽  
Krishnendu Roy ◽  
Agnes Juhasz ◽  
Yongzhong Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Nadph Oxidase ◽  
Cancer Cells ◽  
Human Colon ◽  
Interleukin 4 ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Interleukin 13 ◽  
Nadph Oxidase 1 ◽  
Human Colon Cancer Cells

scholarly journals A Novel and Specific NADPH Oxidase-1 (Nox1) Small-Molecule Inhibitor Blocks the Formation of Functional Invadopodia in Human Colon Cancer Cells

2010 ◽  
Vol 5 (10) ◽  
pp. 981-993 ◽  
Author(s):  
Davide Gianni ◽  
Nicolas Taulet ◽  
Hui Zhang ◽  
Celine DerMardirossian ◽  
Jeremy Kister ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Nadph Oxidase ◽  
Cancer Cells ◽  
Small Molecule ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Molecule Inhibitor ◽  
Nadph Oxidase 1 ◽  
Human Colon Cancer Cells

scholarly journals Effects of Iodonium Analogs on Nadph Oxidase 1 in Human Colon Cancer Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1757
Author(s):  
Krishnendu K. Roy ◽  
Jiamo Lu ◽  
James H. Doroshow
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Nadph Oxidase ◽  
Cancer Cells ◽  
Chemical Properties ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Nadph Oxidase 1 ◽  
Human Colon Cancer Cells

Recent studies suggest that of the molecules postulated to function as inhibitors of the NADPH oxidase family of enzymes iodonium analogs known to broadly interfere with flavin dehydrogenase function demonstrate mechanistic validity as NADPH oxidase poisons. In recent work, we have produced a series of novel iodonium compounds as putative inhibitors of these oxidases. To evaluate the potential utility of two novel molecules with favorable chemical properties, NSC 740104 and NSC 751140, we compared effects of these compounds to the two standard inhibitors of this class, diphenyleneiodonium and di-2-thienyliodonium, with respect to antiproliferative, cell cycle, and gene expression effects in human colon cancer cells that require the function of NADPH oxidase 1. Both new agents blocked NADPH oxidase-related reactive oxygen production, inhibited tumor cell proliferation, produced a G1/S block in cell cycle progression, and inhibited NADPH oxidase 1 expression at the mRNA and protein levels at low nM concentrations in a fashion similar to or better than the parent molecules. These studies suggest that NSC 740104 and NSC 751140 should be developed further as mechanistic tools to better understand the role of NADPH oxidase inhibition as an approach to the development of novel therapeutic agents for colon cancer.

scholarly journals Cholic Acid Stimulates MMP-9 in Human Colon Cancer Cells via Activation of MAPK, AP-1, and NF-κB Activity

2020 ◽  
Vol 21 (10) ◽  
pp. 3420
Author(s):  
Shinan Li ◽  
Trong Thuan Ung ◽  
Thi Thinh Nguyen ◽  
Dhiraj Kumar Sah ◽  
Seon Young Park ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Nadph Oxidase ◽  
Cancer Cells ◽  
P38 Mapk ◽  
Cell Invasion ◽  
Human Colon ◽  
Ros Production ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

Matrix metalloproteinase-9 (MMP-9) plays a crucial role in cell invasion and cancer metastasis. In this study, we showed that cholic acid (CA), a major primary bile acid, can induce MMP-9 expression in colon cancer HT29 and SW620 cells. CA increased reactive oxygen species (ROS) production and also activated phosphorylation of ERK1/2, JNK, and p38 MAPK. Specific inhibitors and mutagenesis studies showed that ERK1/2 and JNK functioned as upstream signals in the activation of AP-1, and p38 MAPK functioned as an upstream signal in the activation of NF-κB. N-acetyl-L-cysteine (NAC, an ROS scavenger) and diphenyleneiodonium chloride (DPI, an NADPH oxidase inhibitor) inhibited CA-induced activation of ERK1/2, JNK, and p38 MAPK, indicating that ROS production by NADPH oxidase could be the furthest upstream signal in MMP-9 expression. Colon cancer cells pretreated with CA showed remarkably enhanced invasiveness. Such enhancement was partially abrogated by MMP-9-neutralizing antibodies. These results demonstrate that CA could induce MMP-9 expression via ROS-dependent ERK1/2, JNK-activated AP-1, and p38-MAPK-activated NF-κB signaling pathways, which in turn stimulate cell invasion in human colon cancer cells.

Leptin is a growth factor for human colon cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A493-A493
Author(s):  
J HARDWICK ◽  
G VANDENBRINK ◽  
S VANDEVENTER ◽  
M PEPPELENBOSCH
Keyword(s):  
Colon Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells
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