scholarly journals The organotelluride catalyst LAB027 prevents colon cancer growth in the mice

2011 ◽  
Vol 2 (8) ◽  
pp. e191-e191 ◽  
Author(s):  
R Coriat ◽  
W Marut ◽  
M Leconte ◽  
L B Ba ◽  
A Vienne ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Growth

VEGF and Colon Cancer Growth Beyond Angiogenesis: Does VEGF Directly Mediate Colon Cancer Growth Via a Non-angiogenic Mechanism?

2014 ◽  
Vol 20 (7) ◽  
pp. 1041-1044 ◽  
Author(s):  
Amrita Ahluwalia ◽  
Michael Jones ◽  
Tamara Matysiak-Budnik ◽  
Andrzej Tarnawski
Keyword(s):  
Colon Cancer ◽  
Cancer Growth

Human α-Defensin 5 suppressed Colon Cancer Growth by Targeting PI3K pathway

2021 ◽  
pp. 112809
Author(s):  
Qiao Qiao ◽  
Ruixia Bai ◽  
Wanying Song ◽  
Haining Gao ◽  
Minyu Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Pi3k Pathway ◽  
Cancer Growth

scholarly journals Deoxycholic Acid Activates β-Catenin Signaling Pathway and Increases Colon Cell Cancer Growth and Invasiveness

2004 ◽  
Vol 15 (5) ◽  
pp. 2156-2163 ◽  
Author(s):  
Rama Pai ◽  
Andrzej S. Tarnawski ◽  
Teresa Tran
Keyword(s):  
Colon Cancer ◽  
Cyclin D1 ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cancer Growth ◽  
Cancer Cell Proliferation ◽  
Cancer Cell Growth ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Secondary Bile Acids

Colorectal cancer is often lethal when invasion and/or metastasis occur. Tumor progression to the metastatic phenotype is mainly dependent on tumor cell invasiveness. Secondary bile acids, particularly deoxycholic acid (DCA), are implicated in promoting colon cancer growth and progression. Whether DCA modulates β-catenin and promotes colon cancer cell growth and invasiveness remains unknown. Because β-catenin and its target genes urokinase-type plasminogen activator receptor (uPAR) and cyclin D1 are overexpressed in colon cancers, and are linked to cancer growth, invasion, and metastasis, we investigated whether DCA activates β-catenin signaling and promotes colon cancer cell growth and invasiveness. Our results show that low concentrations of DCA (5 and 50 μM) significantly increase tyrosine phosphorylation of β-catenin, induce urokinase-type plasminogen activator, uPAR, and cyclin D1 expression and enhance colon cancer cell proliferation and invasiveness. These events are associated with a substantial loss of E-cadherin binding to β-catenin. Inhibition of β-catenin with small interfering RNA significantly reduced DCA-induced uPAR and cyclin D1 expression. Blocking uPAR with a neutralizing antibody significantly suppressed DCA-induced colon cancer cell proliferation and invasiveness. These findings provide evidence for a novel mechanism underlying the oncogenic effects of secondary bile acids.

scholarly journals Noncoding Effects of Circular RNA CCDC66 Promote Colon Cancer Growth and Metastasis

2017 ◽  
Vol 77 (9) ◽  
pp. 2339-2350 ◽  
Author(s):  
Kuei-Yang Hsiao ◽  
Ya-Chi Lin ◽  
Sachin Kumar Gupta ◽  
Ning Chang ◽  
Laising Yen ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Circular Rna ◽  
Cancer Growth

scholarly journals Circular RNA hsa_circ_000984 promotes colon cancer growth and metastasis by sponging miR-106b

Oncotarget ◽  
2017 ◽  
Vol 8 (53) ◽  
pp. 91674-91683 ◽  
Author(s):  
Xiao-Wu Xu ◽  
Bo-An Zheng ◽  
Zhi-Ming Hu ◽  
Zhen-Yuan Qian ◽  
Chao-Jie Huang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Circular Rna ◽  
Cancer Growth

scholarly journals Blocking AMPK/ULK1-dependent autophagy promoted apoptosis and suppressed colon cancer growth

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jing Liu ◽  
Shuaiyu Long ◽  
Huanan Wang ◽  
Nannan Liu ◽  
Chuchu Zhang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Therapeutic Option ◽  
Tumor Xenograft ◽  
Cancer Growth ◽  
Antitumor Effects ◽  
Obvious Effect ◽  
Evolutionarily Conserved ◽  
Induced Apoptosis

Abstract Background Autophagy is an evolutionarily conserved process through which cells degrade and recycle cytoplasm. The relation among autophagy, apoptosis and tumor is highly controversial until now and the molecular mechanism is poorly understood. Methods Cell viability and apoptosis were detected by CCK8, crystal violet staining, Hoechst333342 staining and flow cytometry. The expression of AMPK and ULK1 was analyzed by western blotting. Colon cancer growth suppression by NVP-BEZ235 or CQ in vivo was studied in a tumor xenograft mouse model. Results Our previous study revealed that NVP-BEZ235 suppressed colorectal cancer growth via inducing apoptosis, however later, we found it also initiated autophagy simultaneously. In this present study, our results show that NVP-BEZ235 induced autophagy through AMPK/ULK1 pathway in colon cancer cells. Blocking autophagy by knocking down AMPK or ULK1 inhibited cell proliferation and further promoted NVP-BEZ235 induced apoptosis. Meantime, the autophagy inhibitor chloroquine (CQ) shows obvious effect on inhibiting cell proliferation but not on inducing apoptosis, while it significantly increased NVP-BEZ235 induced apoptosis. Furthermore, the combinational therapy of NVP-BEZ235 and CQ shows synergistic antitumor effects in colon cancer in vivo. Conclusion NVP-BEZ235 induced AMPK/ULK1-dependent autophagy. Targeting this autophagy suppressed colon cancer growth through further promoting apoptosis, which is a potential therapeutic option for clinical patients.

scholarly journals Tandutinib Inhibits the Akt/mTOR Signaling Pathway to Inhibit Colon Cancer Growth

2013 ◽  
Vol 12 (5) ◽  
pp. 598-609 ◽  
Author(s):  
Sivapriya Ponnurangam ◽  
David Standing ◽  
Parthasarathy Rangarajan ◽  
Dharmalingam Subramaniam
Keyword(s):  
Colon Cancer ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Cancer Growth ◽  
Mtor Signaling Pathway

Abstract 2819: Temsirolimus inhibits colon cancer growth in vitro and in vivo

2012 ◽  
Author(s):  
Manabu Kaneko ◽  
Hiroaki Nozawa ◽  
Nelson H. Tsuno ◽  
Kazushige Kawai ◽  
Kazuhito Sasaki ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Growth
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