Butyrate suppresses proliferation and migration of RKO colon cancer cells though regulating endocan expression by MAPK signaling pathway

2013 ◽  
Vol 62 ◽  
pp. 892-900 ◽  
Author(s):  
Li Zuo ◽  
Man Lu ◽  
Qing Zhou ◽  
Wei Wei ◽  
Yuan Wang
2017 ◽  
Vol 141 (8) ◽  
pp. 1614-1629 ◽  
Author(s):  
Khondoker Jahengir Alam ◽  
Ji-Su Mo ◽  
Seol-Hee Han ◽  
Won-Cheol Park ◽  
Hun-Soo Kim ◽  
...  

2017 ◽  
Vol 402 ◽  
pp. 100-109 ◽  
Author(s):  
Yoshiaki Nakamura ◽  
Naoko Hattori ◽  
Naoko Iida ◽  
Satoshi Yamashita ◽  
Akiko Mori ◽  
...  

2021 ◽  
Author(s):  
Fanyu Zeng ◽  
Jie Zhang ◽  
Qianqian Liu ◽  
Shuya Yang ◽  
Xueqing Zhou ◽  
...  

Abstract Breast cancer is the most common invasive malignancy. In 2020, the number of new cases of breast cancer worldwide has replaced lung cancer as the No.1 cancer in the global. Breast cancer is the leading cause of cancer death among women worldwide. Mammary tumorigenesis is severely linked to obesity, one potential connection is chemerin. Chemerin is a chemoattractant protein secreted by adipocytes, which contributes to the progression of breast cancer. Cell proliferation, migration, and invasion are cellular processes associated with various stages of metastasis. These processes are associated with mitogen-activated protein kinase (MAPK) signaling pathway. In this study, human breast cancer cell lines MCF-7 and MDA-MB-231were utilized to determine the effect of chemerin on cell proliferation, migration, and key proteins of MAPK signaling pathway. We found that chemerin promoted cell proliferation and migration in a concentration-dependent manner. Interestingly, these effects of chemerin were through promoting the proteins phosphorylation of ATF2 and ERK1/2 but not p38, in MAPK signaling pathway. Specific inhibitors of JNK and ERK1/2 pathway showed that the effect exerted by chemerin in cell proliferation and migration in breast cancer cells was dependent on these proteins. Our findings suggest that chemerin promotes the development of mammary cancer cells through JNK and ERK signaling pathways.


2021 ◽  
Author(s):  
Daniella Paiva Bonfim ◽  
Celso Vataru Nakamura ◽  
João Xavier Araújo Júnior ◽  
Greisiele Lorena Pessini ◽  
Paulo Emílio Correa Leite ◽  
...  

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Yong Ji ◽  
Yiqian Liu ◽  
Changchun Sun ◽  
Lijiang Yu ◽  
Zhao Wang ◽  
...  

AbstractAs a result of mutations in the upstream components of the Wnt/β-catenin signaling pathway, this cascade is abnormally activated in colon cancer. Hence, identifying the activation mechanism of this pathway is an urgent need for the treatment of colon cancer. Here, we found an increase in ADCK1 (AarF domain-containing kinase 1) expression in clinical specimens of colon cancer and animal models. Upregulation of ADCK1 expression promoted the colony formation and infiltration of cancer cells. Downregulation of ADCK1 expression inhibited the colony formation and infiltration of cancer cells, in vivo tumorigenesis, migration, and organoid formation. Molecular mechanistic studies demonstrated that ADCK1 interacted with TCF4 (T-cell factor 4) to activate the β-catenin/TCF signaling pathway. In conclusion, our research revealed the functions of ADCK1 in the development of colon cancer and provided potential therapeutic targets.


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