scholarly journals Docosahexaenoic fatty acid (DHA) in the regulation of colon cell growth and cell death: A review

2012 ◽  
Vol 156 (3) ◽  
pp. 186-199 ◽  
Author(s):  
Belma Skender ◽  
Alena Hyrslova Vaculova ◽  
Jirina Hofmanova
Keyword(s):  
Cell Death ◽  
Fatty Acid ◽  
Cell Growth ◽  
Colon Cell ◽  
Docosahexaenoic Fatty Acid

scholarly journals Fatty Acid Hydroperoxides and H2O2 in the Execution of Hypersensitive Cell Death in Tobacco Leaves

2005 ◽  
Vol 138 (3) ◽  
pp. 1516-1526 ◽  
Author(s):  
Jean-Luc Montillet ◽  
Sangpen Chamnongpol ◽  
Christine Rustérucci ◽  
James Dat ◽  
Brigitte van de Cotte ◽  
...  
Keyword(s):  
Cell Death ◽  
Fatty Acid ◽  
Hypersensitive Cell Death ◽  
Tobacco Leaves ◽  
Fatty Acid Hydroperoxides

scholarly journals LONP1 and ClpP cooperatively regulate mitochondrial proteostasis for cancer cell survival

Oncogenesis ◽  
2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Yu Geon Lee ◽  
Hui Won Kim ◽  
Yeji Nam ◽  
Kyeong Jin Shin ◽  
Yu Jin Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Cell Survival ◽  
Cancer Cell ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Tca Cycle ◽  
Mitochondrial Matrix ◽  
Mitochondrial Functions ◽  
Cancer Cell Survival

AbstractMitochondrial proteases are key components in mitochondrial stress responses that maintain proteostasis and mitochondrial integrity in harsh environmental conditions, which leads to the acquisition of aggressive phenotypes, including chemoresistance and metastasis. However, the molecular mechanisms and exact role of mitochondrial proteases in cancer remain largely unexplored. Here, we identified functional crosstalk between LONP1 and ClpP, which are two mitochondrial matrix proteases that cooperate to attenuate proteotoxic stress and protect mitochondrial functions for cancer cell survival. LONP1 and ClpP genes closely localized on chromosome 19 and were co-expressed at high levels in most human cancers. Depletion of both genes synergistically attenuated cancer cell growth and induced cell death due to impaired mitochondrial functions and increased oxidative stress. Using mitochondrial matrix proteomic analysis with an engineered peroxidase (APEX)-mediated proximity biotinylation method, we identified the specific target substrates of these proteases, which were crucial components of mitochondrial functions, including oxidative phosphorylation, the TCA cycle, and amino acid and lipid metabolism. Furthermore, we found that LONP1 and ClpP shared many substrates, including serine hydroxymethyltransferase 2 (SHMT2). Inhibition of both LONP1 and ClpP additively increased the amount of unfolded SHMT2 protein and enhanced sensitivity to SHMT2 inhibitor, resulting in significantly reduced cell growth and increased cell death under metabolic stress. Additionally, prostate cancer patients with higher LONP1 and ClpP expression exhibited poorer survival. These results suggest that interventions targeting the mitochondrial proteostasis network via LONP1 and ClpP could be potential therapeutic strategies for cancer.

Lipid biomarkers of glioma cell growth arrest and cell death detected by 1 H magic angle spinning MRS

2012 ◽  
Vol 25 (11) ◽  
pp. 1253-1262 ◽  
Author(s):  
Ladan Mirbahai ◽  
Martin Wilson ◽  
Christopher S. Shaw ◽  
Carmel McConville ◽  
Roger D. G. Malcomson ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Glioma Cell ◽  
Growth Arrest ◽  
Magic Angle Spinning ◽  
Lipid Biomarkers ◽  
Magic Angle ◽  
Cell Growth Arrest ◽  
Angle Spinning

Inhibition of 5-lipoxygenase induces cell death in anti-inflammatory fatty acid-treated HL-60 cells

2004 ◽  
Vol 28 (5) ◽  
pp. 308-314 ◽  
Author(s):  
RC Gillis ◽  
BJ Daley ◽  
BL Enderson ◽  
MD Karlstad
Keyword(s):  
Cell Death ◽  
Fatty Acid ◽  
Anti Inflammatory

Pyridaben leads to inhibition of cell growth and induction of cell death through intracellular mechanisms in early pregnancy

2021 ◽  
Vol 171 ◽  
pp. 104733
Author(s):  
Hyocheol Bae ◽  
Seungkwon You ◽  
Whasun Lim ◽  
Gwonhwa Song
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Early Pregnancy ◽  
Intracellular Mechanisms

Connexins and their channels in cell growth and cell death

2006 ◽  
Vol 18 (5) ◽  
pp. 592-600 ◽  
Author(s):  
Mathieu Vinken ◽  
Tamara Vanhaecke ◽  
Peggy Papeleu ◽  
Sarah Snykers ◽  
Tom Henkens ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth

scholarly journals Mechanism of Pterostilbene-Induced Cell Death in HT-29 Colon Cancer Cells

Molecules ◽  
2022 ◽  
Vol 27 (2) ◽  
pp. 369
Author(s):  
Joanna Wawszczyk ◽  
Katarzyna Jesse ◽  
Sławomir Smolik ◽  
Małgorzata Kapral
Keyword(s):  
Colon Cancer ◽  
Cell Death ◽  
Cell Growth ◽  
Cancer Cells ◽  
Biological Activities ◽  
Therapeutic Option ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Inhibition Of Proliferation ◽  
Ht 29

Pterostilbene is a dietary phytochemical that has been found to possess several biological activities, such as antioxidant and anti-inflammatory. Recent studies have shown that it exhibits the hallmark characteristics of an anticancer agent. The aim of the study was to investigate the anticancer activity of pterostilbene against HT-29 human colon cancer cells, focusing on its influence on cell growth, differentiation, and the ability of this stilbene to induce cell death. To clarify the mechanism of pterostilbene activity against colon cancer cells, changes in the expression of several genes and proteins that are directly related to cell proliferation, signal transduction pathways, apoptosis, and autophagy were also evaluated. Cell growth and proliferation of cells exposed to pterostilbene (5–100 µM) were determined by SRB and BRDU assays. Flow cytometric analyses were used for cell cycle progression. Further molecular investigations were performed using quantitative real-time RT-PCR. The expression of the signaling proteins studied was determined by the ELISA method. The results revealed that pterostilbene inhibited proliferation and induced the death of HT-29 colon cancer cells. Pterostilbene, depending on concentration, caused inhibition of proliferation, G1 cell arrest, and/or triggered apoptosis in HT-29 cells. These effects were mediated by the down-regulation of the STAT3 and AKT kinase pathways. It may be concluded that pterostilbene could be considered as a potential therapeutic option in the treatment of colon cancer in the future.

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