Normal human colon cells suppress malignancy when fused with colon cancer cells

1990 ◽  
Vol 26 (11) ◽  
pp. 1095-1100 ◽  
Author(s):  
Teresa L. Johnson ◽  
Mary Pat Moyer
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Colon Cells ◽  
Normal Human

scholarly journals CHK Methylation Is Elevated in Colon Cancer Cells and Contributes to the Oncogenic Properties

2021 ◽  
Vol 9 ◽  
Author(s):  
Shudong Zhu ◽  
Yan Zhu ◽  
Qiuwen Wang ◽  
Yi Zhang ◽  
Xialing Guo
Keyword(s):  
Dna Methylation ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Dna Methyltransferases ◽  
Colon Cancer Cells ◽  
Normal Colon ◽  
Human Colon Cancer ◽  
Colon Cells ◽  
Matrigel Invasion

Src is an important oncogene that plays key roles in multiple signal transduction pathways. Csk-homologous kinase (CHK) is a kinase whose molecular roles are largely uncharacterized. We previously reported expression of CHK in normal human colon cells, and decreased levels of CHK protein in colon cancer cells leads to the activation of Src (Zhu et al., 2008). However, how CHK protein expression is downregulated in colon cancer cells has been unknown. We report herein that CHK mRNA was decreased in colon cancer cells as compared to normal colon cells, and similarly in human tissues of normal colon and colon cancer. Increased levels of DNA methylation at promotor CpG islands of CHK gene were observed in colon cancer cells and human colon cancer tissues as compared to their normal healthy counterparts. Increased levels of DNA methyltransferases (DNMTs) were also observed in colon cancer cells and tissues. DNA methylation and decreased expression of CHK mRNA were inhibited by DNMT inhibitor 5-Aza-CdR. Cell proliferation, colony growth, wound healing, and Matrigel invasion were all decreased in the presence of 5-Aza-CdR. These results suggest that increased levels of DNA methylation, possibly induced by enhanced levels of DNMT, leads to decreased expression of CHK mRNA and CHK protein, promoting increased oncogenic properties in colon cancer cells.

scholarly journals Resveratrol overcomes TRAIL resistance in human colon cancer cells

2015 ◽  
Vol 10 (3) ◽  
pp. 568
Author(s):  
Xiao-Bing Li ◽  
Yun-Gang Deng ◽  
Jia-Ping Hu ◽  
Zhi Wang ◽  
Rong-Zhen Xie ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Trail Receptors ◽  
Normal Human ◽  
Induced Apoptosis ◽  
Human Colon Cancer Cells

<p><strong>Abstract</strong></p> <p><strong> </strong></p> Resveratrol is a stilbenoid compound, and a promising potent chemopreventive bioactive agent. Here, we showed for the first time that the combined treatment with resveratrol and TRAIL drastically induced apoptosis in human colon cancer cells when compared to single treatments. Further, resveratrol markedly up-regulated TRAIL receptors, DR5 and DR4 and the results revealed that DR5 siRNA efficiently blocked apoptosis induced by the co-treatment with resveratrol and TRAIL, indicating that DR5 up-regulation by resveratrol helps to enhance TRAIL actions. In addition, the combined effect were tested on normal human cells. All the obtained results suggested that resveratrol is very useful for TRAIL-based treatments for cancer.

scholarly journals A Nudibranch Marine Extract Selectively Chemosensitizes Colorectal Cancer Cells by Inducing ROS-Mediated Endoplasmic Reticulum Stress

2021 ◽  
Vol 12 ◽  
Author(s):  
Verónica Ruiz-Torres ◽  
Nicholas Forsythe ◽  
Almudena Pérez-Sánchez ◽  
Sandra Van Schaeybroeck ◽  
Enrique Barrajón-Catalán ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cancer Cells ◽  
Human Colon ◽  
Resistance Mechanisms ◽  
Colon Cancer Cells ◽  
Colon Cells ◽  
Lower Effect ◽  
The Unfolded Protein Response

The present study shows the putative antiproliferative mechanism of action of the previously analytically characterized nudibranch extract ( Dolabella auricularia, NB) and its different effects in colon cancer cells vs. nontumor colon cells. NB extract increased the accumulation of reactive oxygen species (ROS) and increased endoplasmic reticulum (ER) stress via stimulation of the unfolded protein response. Stress scavengers, N-acetylcysteine (NAC) and 4-phenylbutyric acid (4-PBA), decreased the stress induced by NB. The results showed that NB extract increased ER stress through overproduction of ROS in superinvasive colon cancer cells, decreased their resistance threshold, and produced a nonreturn level of ER stress, causing DNA damage and cell cycle arrest, which prevented them from achieving hyperproliferative capacity and migrating to and invading other tissues. On the contrary, NB extract had a considerably lower effect on nontumor human colon cells, suggesting a selective effect related to stress balance homeostasis. In conclusion, our results confirm that the growth and malignancy of colon cancer cells can be decreased by marine compounds through the modification of one of the most potent resistance mechanisms present in tumor cells; this characteristic differentiates cancer cells from nontumor cells in terms of stress balance.

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

SENP1 participates in Irinotecan resistance in human colon cancer cells

2021 ◽  
Author(s):  
Ming‐Cheng Chen ◽  
Do Chi Nhan ◽  
Chiung‐Hung Hsu ◽  
Tso‐Fu Wang ◽  
Chi‐Cheng Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells
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