Colorectal Cancer Cells
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2021 ◽  
Vol 46 ◽  
pp. S553
Author(s):  
A. Pakiet ◽  
A. Mika ◽  
J. Kobiela ◽  
A. Czumaj ◽  
T. Śledziński

2021 ◽  
Author(s):  
Min Zhang ◽  
Jing Wang ◽  
Hanming Gu

Functional mitochondria are crucial to the development and metastasis of cancer cells. C14orf159 is an important mitochondrial protein and is associated with the proliferation of cancer cells. In our study, we aim to identify essential signaling pathways and biological processes in the knockout of C14orf159 in colorectal cancer cells. The GSE167947 dataset was produced by using the Illumina HiSeq 2500 (Homo sapiens). The KEGG and GO analyses showed that biological processes “Staphylococcus aureus infection” and “Systemic lupus erythematosus” are the most important processes in the loss of C14orf159. Moreover, we identified a variety of genes by constructing the PPI network, which includes Albumin, Brain derived neurotrophic factor, and Matrix metallopeptidase 9. Therefore, our study provides insights into the treatment of colorectal cancer by targeting mitochondria.


2021 ◽  
Author(s):  
Patricia Dias-Carvalho ◽  
Flavia Martins ◽  
Susana Mendonca ◽  
Andreia Ribeiro ◽  
Ana Luisa Machado ◽  
...  

Genetic alterations influence the malignant potential of cancer cells, and so does the tumor microenvironment. Herein, we combined the study of KRAS oncogenic effects in colorectal cancer cells with the influence of fibroblasts derived factors. Results revealed that mutant KRAS regulates cell fate through both autonomous and non autonomous signaling mechanisms. Specifically, processes such as proliferation and cell-cell aggregation were autonomously controlled by mutant KRAS independently of the stimulation with fibroblasts conditioned media. However, cancer cell invasion revealed to be a KRAS dependent non-autonomous effect, resulting from the cooperation between fibroblasts-derived HGF and mutant KRAS regulation of C-MET expression. C-MET downregulation upon KRAS silencing rendered cells less responsive to HGF and thus less invasive. Yet, in one cell line, KRAS inhibition triggered invasion upon stimulation with fibroblasts conditioned media. Inhibition of PIK3CA oncogene did not promoted invasion, thus showing a KRAS specific effect. Moreover, the invasive capacity also depended on the HGF-C-MET axis. Overall, our study awards oncogenic KRAS an important role in modulating the response to fibroblast-secreted factors either by promoting or impairing invasion, and depicts the HGF-C-MET axis as a putative therapeutic target to impair the invasive properties of mutant KRAS cancer cells.


2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Wenli Chen ◽  
Guangli Dai ◽  
Yike Qian ◽  
Lian Wen ◽  
Xueqing He ◽  
...  

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