scholarly journals Norcantharidin Suppresses Colon Cancer Cell Epithelial-Mesenchymal Transition by Inhibiting the αvβ6-ERK-Ets1 Signaling Pathway

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Cheng Peng ◽  
Zequn Li ◽  
Zhengchuan Niu ◽  
Wei Niu ◽  
Zongquan Xu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Colon Cancer Cell ◽  
Mesenchymal Transition

Ginsenoside Rg3 Suppresses Epithelial-Mesenchymal Transition via Downregulating Notch-Hes1 Signaling in Colon Cancer Cells

2020 ◽  
pp. 1-19
Author(s):  
Xiao Li ◽  
Wei Liu ◽  
Chong Geng ◽  
Tingting Li ◽  
Yanni Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Ginsenoside Rg3 ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
E Cadherin

Invasion and metastasis are the major causes leading to the high mortality of colon cancer. Ginsenoside Rg3 (Rg3), as a bioactive ginseng compound, is suggested to possess antimetastasis effects in colon cancer. However, the underlying molecular mechanisms remain unclear. In this study, we reported that Rg3 could effectively inhibit colon cancer cell invasion and metastasis through in vivo and in vitro studies. In addition, Rg3 suppressed the epithelial–mesenchymal transition (EMT) of HCT15 cells and SW48 cells evidenced by detecting EMT related markers E-cadherin, vimentin, and snail expression. Furthermore, inhibition of Notch signaling by LY411,575 or specific Hes1 siRNA obviously repressed colon cancer cell migration and metastasis, and induced increase in E-cadherin and decrease in vimentin and snail. Meanwhile, the expression of NICD and Hes1 was obviously decreased in the presence of Rg3. However, Rg3 failed to suppress EMT in Hes1 overexpressed colon cancer cells. In particular, Rg3 significantly reversed IL-6-induced EMT promotion and blocked IL-6- induced NICD and Hes1 upregulations. Overall, these findings suggested that Rg3 could inhibit colon cancer migration and metastasis via suppressing Notch-Hes1-EMT signaling.

Curcumin reverses irinotecan resistance in colon cancer cell by regulation of epithelial–mesenchymal transition

2018 ◽  
Vol 29 (4) ◽  
pp. 334-340 ◽  
Author(s):  
Chunhong Zhang ◽  
Yangjie Xu ◽  
Haowen Wang ◽  
Gang Li ◽  
Han Yan ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Colon Cancer Cell ◽  
Mesenchymal Transition

scholarly journals MicroRNA-4284 inhibits colon cancer epithelial-mesenchymal transition by down-regulating Perilipin 5

STEMedicine ◽  
2021 ◽  
Vol 2 (6) ◽  
pp. e85
Author(s):  
Xiaofei Miao ◽  
Zengyao Li ◽  
Ye Zhang ◽  
Tong Wang
Keyword(s):  
Colon Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Cell Lines ◽  
Colon Cancer Cell ◽  
Metastatic Colon Cancer ◽  
Mesenchymal Transition ◽  
Colon Cancer Cell Lines ◽  
Perilipin 5

Background: MicroRNA (miR) has been suggested in the development of several types of cancer; yet, the exact function of miR-4284 in colon cancer remains elusive. Methods: MiR-4284 expression was assessed in normal colon cell line CCD-18Co, and HT-29 and SW480 cell lines representing human colon cancer. Potential target gene of miR-4284 was predicted using TargetScanHuman, and experimentally verified using luciferase report assay. Wound-healing, cell invasion and attachment were evaluated to determine the effect of miR-4284 on the migration, invasion, and metastatic properties of colon cancer cell lines. Expression of epithelial-mesenchymal transition (EMT) phenotypic protein hallmarks, including N-cadherin, E-cadherin, as well as Vimentin, was also evaluated. Results: MiR-4284 was significantly decreased in colon cancer cell lines, and Perilipin 5 (PLIN5) was found to be directly targeted by miR-4284. Ectopic expression of miR-4284 significantly reduced endogenous expression level of PLIN5 in colon cancer cell lines, suppressing migration, invasion, and metastatic phenotypes. In addition, re-introducing miR-4284 reversed the expression profile of EMT markers. Conclusion: Our findings for the first time identify miR-4284 as an anti-tumor miRNA in colon cancer, which acts to reduce PLIN5 and inhibit EMT, leading to inhibited colon cancer tumorigenesis. These results highlight the potential of miR-4284 as a therapeutic target in metastatic colon cancer.

Sign in / Sign up

Export Citation Format

Share Document