MicroRNA‐188‐5p promotes apoptosis and inhibits cell proliferation of breast cancer cells via the MAPK signaling pathway by targeting Rap2c

2019 ◽  
Vol 235 (3) ◽  
pp. 2389-2402 ◽  
Author(s):  
Xinying Zhu ◽  
Jinxia Qiu ◽  
Tao Zhang ◽  
Yaping Yang ◽  
Shuai Guo ◽  
...  
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 ◽  
Vol 22 (22) ◽  
pp. 12229
Author(s):  
Junfeng Ke ◽  
Wenzhao Han ◽  
Fanwei Meng ◽  
Feng Guo ◽  
Yuhong Wang ◽  
...  

Although some breast cancer patients die due to tumor metastasis rather than from the primary tumor, the molecular mechanism of metastasis remains unclear. Therefore, it is necessary to inhibit breast cancer metastasis during cancer treatment. In this case, after designing and synthesizing CTI-2, we found that CTI-2 treatment significantly reduced breast cancer cell metastasis in vivo and in vitro. Notably, with the treatment of CTI-2 in breast cancer cells, the expression level of E-cadherin increased, while the expression level of N-cadherin and vimentin decreased. In addition, after CTI-2 treatment, those outflow levels for p-ERK, p-p38, and p-JNK diminished, while no significant changes in the expression levels of ERK, JNK, or p38 were observed. Our conclusion suggested that CTI-2 inhibits the epithelial-mesenchymal transition (EMT) of breast carcinoma cells by inhibiting the activation of the mitogen-activated protein kinase (MAPK) signaling pathway, thereby inhibiting the metastasis of breast tumor cells. Therefore, we believe that CTI-2 is another candidate for breast tumor medication.


2008 ◽  
Vol 118 (2) ◽  
pp. 281-291 ◽  
Author(s):  
Manabu Watanabe ◽  
Nozomi Miyajima ◽  
Maki Igarashi ◽  
Yoshifumi Endo ◽  
Natsuko Watanabe ◽  
...  

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