Hyperthermia in combination with oxidative stress induces autophagic cell death in HT-29 colon cancer cells

2008 ◽  
Vol 32 (7) ◽  
pp. 715-723 ◽  
Author(s):  
F CHEN ◽  
C WANG ◽  
E KIM ◽  
L HARRISON
Molecules ◽  
2022 ◽  
Vol 27 (2) ◽  
pp. 369
Author(s):  
Joanna Wawszczyk ◽  
Katarzyna Jesse ◽  
Sławomir Smolik ◽  
Małgorzata Kapral

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.


Phytomedicine ◽  
2015 ◽  
Vol 22 (5) ◽  
pp. 536-544 ◽  
Author(s):  
Tao Hu ◽  
Lin Wang ◽  
Lin Zhang ◽  
Lan Lu ◽  
Jing Shen ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e63641 ◽  
Author(s):  
Shun X. Ren ◽  
Jin Shen ◽  
Alfred S. L. Cheng ◽  
Lan Lu ◽  
Ruby L. Y. Chan ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Tamotsu Tsukahara ◽  
Yoshikazu Matsuda ◽  
Hisao Haniu

Our previous study demonstrated that PTB-associated splicing factor (PSF) is an important regulator of cell death and plays critical roles in the survival and growth of colon cancer cells. However, the molecular mechanism that activates these downstream signaling events remains unknown. To address this issue, we investigated the effects of PSF knockdown in two different colon cancer cell lines, DLD-1 and HT-29. We found that knockdown of PSF markedly decreased the autophagic molecule LC3B in DLD-1 cells but not in HT-29 cells. Furthermore, DLD-1 cells were more susceptible to PSF knockdown-induced cell growth inhibition and apoptosis than HT-29 cells. This susceptibility is probably a result of LC3B inhibition, given the known relationship between autophagy and apoptosis. C3B is associated with a number of physiological processes, including cell growth and apoptotic cell death. Our results suggest that autophagy is inhibited by PSF knockdown and that apoptosis and cell growth inhibition may act together to mediate the PSF-LC3B signaling pathway. Furthermore, we found that the peroxisome proliferator-activated receptor gamma (PPARγ)-PSF complex induced LC3B downregulation in DLD-1 cells. The results of this study identify a new physiological role for the PSF-LC3B axis as a potential endogenous modulator of colon cancer treatment.


2016 ◽  
Vol 61 (2) ◽  
pp. 1600437 ◽  
Author(s):  
Yueliang Zhao ◽  
Daming Fan ◽  
Zong-Ping Zheng ◽  
Edmund T.S. Li ◽  
Feng Chen ◽  
...  

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