IL-1α secreted by colon cancer cells enhances angiogenesis: The relationship between IL-1α release and tumor cells' potential for liver metastasis

2009 ◽  
Vol 99 (6) ◽  
pp. 361-367 ◽  
Author(s):  
Yoichi Matsuo ◽  
Hirozumi Sawai ◽  
Jiachi Ma ◽  
Donghui Xu ◽  
Nobuo Ochi ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Liver Metastasis ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Colon Cancer Cells ◽  
The Relationship

Co-migration of colon cancer cells and CAFs induced by TGFβ1 enhances liver metastasis

2015 ◽  
Vol 359 (3) ◽  
pp. 829-839 ◽  
Author(s):  
Idoia Gonzalez-Zubeldia ◽  
Javier Dotor ◽  
Miriam Redrado ◽  
Anne-Marie Bleau ◽  
Irene Manrique ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Liver Metastasis ◽  
Cancer Cells ◽  
Colon Cancer Cells

scholarly journals Down-regulation of PINCH-1 Reduces Expression of EGFR, ERK1/2 and c-Myc, and Leads to Loss of Cell Viability in Colon Cancer Cells

2016 ◽  
Vol 2 (1) ◽  
Author(s):  
Birgitta Holmlund ◽  
Annica Holmqvist
Keyword(s):  
Colon Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Cell Number ◽  
Colon Cancer Cells ◽  
Down Regulation ◽  
Fluorescent Substrate ◽  
Antibody Arrays ◽  
The Relationship

Particularly interesting new cysteine-histidine rich protein (PINCH) is related to poor outcome in colorectal cancers. Here, the relationship between PINCH-1 and cell survival in colon cancer cells was analyzed and the signaling pathways regulated by PINCH-1 by using PINCH-1 siRNA. KM12C cells were treated with PINCH-1 siRNA or control siRNA. Cell number was analyzed by crystal violet staining and caspase-3 activity was assessed using a fluorescent substrate. PINCH-1 extra- and intracellular pathways in KM12C cells were investigated, using phospho-kinase/phospho-receptor tyrosine kinase (RTK) antibody arrays. The expression of c-Myc was evaluated by Quantitative real-time PCR (qPCR) and Western blot analysis. Cell number was significantly decreased (P=0.003) and the caspase-3 activity increased (P=0.019) in PINCH-1 depleted KM12C cultures compared to siRNA cultures. In PINCH-1 silenced KM12C cells, the levels of EGFR and ERK1/2 were significantly decreased (P=0.008, P=0.003, respectively) compared to their controls, as were the c-Myc mRNA and protein expressions (P=0.0073, P=0.0002, respectively). Down-regulation of PINCH-1 reduced the cell survival and lowers the levels of EGFR, ERK1/2 and c-Myc in colon cancer cells. PINCH-1 is essential for cell survival, and may be a future target for anticancer therapy. 

scholarly journals Nrf3 Promotes 5-FU Resistance in Colorectal Cancer Cells via the NF-κB/BCL-2 Signaling Pathway In Vitro and In Vivo

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Bi-Qing Cai ◽  
Wan-Meng Chen ◽  
Jia Zhao ◽  
Wei Hou ◽  
Jian-Cai Tang
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Colon Cancer Cells ◽  
Tumor Drug Resistance ◽  
Colorectal Cancer Cells ◽  
Cancer Tissues ◽  
The Relationship

Increasing evidence indicates that nuclear factor, erythroid 2-like 3 (Nrf3) is connected with tumorigenesis. However, the relationship between Nrf3 and tumor drug resistance remains elusive. In this study, we investigated the effect and mechanism of action by which Nrf3 regulated the sensitivity of colon cancer cells to 5-fluorouracil (5-FU). We found Nrf3 was significantly increased in colon cancer tissues. Furthermore, we observed that Nrf3 knockdown and overexpression can significantly affect the sensitivity of colon cancer cells to 5-FU in vitro and in vivo. Moreover, Nrf3 promoted the expression of RELA, P-RELA, and BCL-2. Inhibition of NF-κB partly reversed the effects of Nrf3 overexpression, resulting in the resistance of colon cancer cells to 5-FU. Overall, the study revealed that Nrf3 was connected to the sensitivity of colon cancer cells to 5-FU, and its possible mechanism was related to the NF-κB signaling pathway, which provided a new target for overcoming the resistance of colon cancer cells to 5-FU.

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