scholarly journals microRNA-16 represses colorectal cancer cell growth in vitro by regulating the p53/survivin signaling pathway

2013 ◽  
Vol 29 (4) ◽  
pp. 1652-1658 ◽  
Author(s):  
QUNYING MA ◽  
XINYING WANG ◽  
ZHAO LI ◽  
BINGSHENG LI ◽  
FENGLI MA ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Colorectal Cancer Cell ◽  
Cancer Cell Growth

ECRG4 as a novel tumor suppressor gene inhibits colorectal cancer cell growth in vitro and in vivo

Tumor Biology ◽  
2016 ◽  
Vol 37 (7) ◽  
pp. 9111-9120 ◽  
Author(s):  
Zhengxu Cai ◽  
Pin Liang ◽  
Jize Xuan ◽  
Jiajia Wan ◽  
Huishu Guo
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Cancer Cell ◽  
Suppressor Gene ◽  
Colorectal Cancer Cell ◽  
Cancer Cell Growth

LYTAK1, a novel TAK1 inhibitor, suppresses KRAS mutant colorectal cancer cell growth in vitro and in vivo

Tumor Biology ◽  
2014 ◽  
Vol 36 (5) ◽  
pp. 3301-3308 ◽  
Author(s):  
Jundong Zhou ◽  
Bing Zheng ◽  
Jiansong Ji ◽  
Fei Shen ◽  
Han Min ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Colorectal Cancer Cell ◽  
Cancer Cell Growth

scholarly journals Adenovirus-mediated expression of SSAT inhibits colorectal cancer cell growth in vitro

2008 ◽  
Vol 29 (5) ◽  
pp. 606-613 ◽  
Author(s):  
Hui SUN ◽  
Bin LIU ◽  
Ya-pei YANG ◽  
Chun-xiao XU ◽  
Yun-fei YAN ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Colorectal Cancer Cell ◽  
Cancer Cell Growth

scholarly journals LKB1 and YAP phosphorylation play important roles in Celastrol-induced β-catenin degradation in colorectal cancer

2019 ◽  
Vol 11 ◽  
pp. 175883591984373 ◽  
Author(s):  
Shuren Wang ◽  
Kai Ma ◽  
Cuiqi Zhou ◽  
Yu Wang ◽  
Guanghui Hu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Transcriptional Activation ◽  
Molecular Mechanisms ◽  
Inhibitory Effect ◽  
Colorectal Cancer Cell ◽  
Cancer Cell Growth

Wnt/β-catenin and Hippo pathways play essential roles in the tumorigenesis and development of colorectal cancer. We found that Celastrol, isolated from Tripterygium wilfordii plant, exerted a significant inhibitory effect on colorectal cancer cell growth in vitro and in vivo, and further unraveled the molecular mechanisms. Celastrol induced β-catenin degradation through phosphorylation of Yes-associated protein (YAP), a major downstream effector of Hippo pathway, and also Celastrol-induced β-catenin degradation was dependent on liver kinase B1 (LKB1). Celastrol increased the transcriptional activation of LKB1, partially through the heat shock factor 1 (HSF1). Moreover, LKB1 activated AMP-activated protein kinase α (AMPKα) and further phosphorylated YAP, which eventually promoted the degradation of β-catenin. In addition, LKB1 deficiency promoted colorectal cancer cell growth and attenuated the inhibitory effect of Celastrol on colorectal cancer growth both in vitro and in vivo. Taken together, Celastrol inhibited colorectal cancer cell growth by promoting β-catenin degradation via the HSF1–LKB1–AMPKα–YAP pathway. These results suggested that Celastrol may potentially serve as a future drug for colorectal cancer treatment.

Molecular Size Fractions of Bay Leaf(Laurus nobilis)Exhibit Differentiated Regulation of Colorectal Cancer Cell Growth In Vitro

2013 ◽  
Vol 65 (5) ◽  
pp. 746-764 ◽  
Author(s):  
Louise Bennett ◽  
Mahinda Abeywardena ◽  
Sharon Burnard ◽  
Santina Forsyth ◽  
Richard Head ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Molecular Size ◽  
Colorectal Cancer Cell ◽  
Laurus Nobilis ◽  
Cancer Cell Growth ◽  
Size Fractions
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