Water Stress Proteins fromNostoc communeVauch. Exhibit Anti-Colon Cancer Activities in Vitro and in Vivo

2015 ◽  
Vol 63 (1) ◽  
pp. 150-159 ◽  
Author(s):  
Songjia Guo ◽  
Shuhua Shan ◽  
Xiaoting Jin ◽  
Zongwei Li ◽  
Zhuoyu Li ◽  
...  
2021 ◽  
Author(s):  
Songjia Guo ◽  
Shuhua Shan ◽  
Haili Wu ◽  
huiqiang hao ◽  
Zhuoyu Li

Abstract Nostoc commune Vauch is a nitrogen-fixing blue-green algae, contains a large number of active molecules with medicinal functions. Our previous study found that a water stress protein (WSP1) from Nostoc commune Vauch and its the recombinant protein (Re-WSP1) exhibited significant anti-colon cancer (CRC) activity both in vitro and in vivo. However, the underlying mechanism remains unknown. In this study, the CCK8 and clonogenic assays showed that Re-WSP1 restrained the colon cancer growth in a dose-dependent manner. Mechanistically, Re-WSP1 inhibited the expression of β-catenin, which was partly reversed by LiCl treatment, demonstrating a key role in Re-WSP1-induced inhibition of cell growth. Quantitative PCR analysis showed that the expression of microRNA-539 (miR-539) was significantly up-regulated upon Re-WSP1 treatment. Moreover, miR-539 negatively regulateed the expression of β-catenin through directly binds to the 3’UTR of β-catenin mRNA. Taken together, our data demonstrate that Re-WSP1 suppresses the CRC growth via miR-539/β-catenin axis, which provides new insights into the molecular mechanisms underlying Re-WSP1 against CRC.


2021 ◽  
Vol 129 (5) ◽  
pp. 053301
Author(s):  
Eric Freund ◽  
Lea Miebach ◽  
Ramona Clemen ◽  
Michael Schmidt ◽  
Amanda Heidecke ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kazim Husain ◽  
Domenico Coppola ◽  
Chung S. Yang ◽  
Mokenge P. Malafa

AbstractThe activation and growth of tumour-initiating cells with stem-like properties in distant organs characterize colorectal cancer (CRC) growth and metastasis. Thus, inhibition of colon cancer stem cell (CCSC) growth holds promise for CRC growth and metastasis prevention. We and others have shown that farnesyl dimethyl chromanol (FDMC) inhibits cancer cell growth and induces apoptosis in vitro and in vivo. We provide the first demonstration that FDMC inhibits CCSC viability, survival, self-renewal (spheroid formation), pluripotent transcription factors (Nanog, Oct4, and Sox2) expression, organoids formation, and Wnt/β-catenin signalling, as evidenced by comparisons with vehicle-treated controls. In addition, FDMC inhibits CCSC migration, invasion, inflammation (NF-kB), angiogenesis (vascular endothelial growth factor, VEGF), and metastasis (MMP9), which are critical tumour metastasis processes. Moreover, FDMC induced apoptosis (TUNEL, Annexin V, cleaved caspase 3, and cleaved PARP) in CCSCs and CCSC-derived spheroids and organoids. Finally, in an orthotopic (cecum-injected CCSCs) xenograft metastasis model, we show that FDMC significantly retards CCSC-derived tumour growth (Ki-67); inhibits inflammation (NF-kB), angiogenesis (VEGF and CD31), and β-catenin signalling; and induces apoptosis (cleaved PARP) in tumour tissues and inhibits liver metastasis. In summary, our results demonstrate that FDMC inhibits the CCSC metastatic phenotype and thereby supports investigating its ability to prevent CRC metastases.


Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 106
Author(s):  
Yeongji Yu ◽  
Hyejin Kim ◽  
SeokGyeong Choi ◽  
JinSuh Yu ◽  
Joo Yeon Lee ◽  
...  

The elimination of the cancer stem cell (CSC) population may be required to achieve better outcomes of cancer therapy. We evaluated stearoyl-CoA desaturase 1 (SCD1) as a novel target for CSC-selective elimination in colon cancer. CSCs expressed more SCD1 than bulk cultured cells (BCCs), and blocking SCD1 expression or function revealed an essential role for SCD1 in the survival of CSCs, but not BCCs. The CSC potential selectively decreased after treatment with the SCD1 inhibitor in vitro and in vivo. The CSC-selective suppression was mediated through the induction of apoptosis. The mechanism leading to selective CSC death was investigated by performing a quantitative RT-PCR analysis of 14 CSC-specific signaling and marker genes after 24 and 48 h of treatment with two concentrations of an inhibitor. The decrease in the expression of Notch1 and AXIN2 preceded changes in the expression of all other genes, at 24 h of treatment in a dose-dependent manner, followed by the downregulation of most Wnt- and NOTCH-signaling genes. Collectively, we showed that not only Wnt but also NOTCH signaling is a primary target of suppression by SCD1 inhibition in CSCs, suggesting the possibility of targeting SCD1 against colon cancer in clinical settings.


Helia ◽  
2004 ◽  
Vol 27 (40) ◽  
pp. 227-236 ◽  
Author(s):  
H. Turhan ◽  
I. Baser

Gut ◽  
2012 ◽  
Vol 62 (4) ◽  
pp. 561-570 ◽  
Author(s):  
Hyun-Seuk Moon ◽  
Xiaowen Liu ◽  
Jutta M Nagel ◽  
John P Chamberland ◽  
Kalliope N Diakopoulos ◽  
...  

2010 ◽  
Vol 45 (9) ◽  
pp. 3702-3708 ◽  
Author(s):  
Shiby Paul ◽  
Cassia S. Mizuno ◽  
Hong Jin Lee ◽  
Xi Zheng ◽  
Sarah Chajkowisk ◽  
...  

2013 ◽  
Vol 144 (5) ◽  
pp. S-166-S-167
Author(s):  
Karen Boland ◽  
Caoimhin Concannon ◽  
Niamh McCawley ◽  
Elaine W. Kay ◽  
Deborah McNamara ◽  
...  

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