Leuconostoc mesenteroides-derived anticancer pharmaceuticals hinder inflammation and cell survival in colon cancer cells by modulating NF-κB/AKT/PTEN/MAPK pathways

2017 ◽  
Vol 94 ◽  
pp. 1094-1100 ◽  
Author(s):  
Sepideh Zununi Vahed ◽  
Abolfazl Barzegari ◽  
Yalda Rahbar Saadat ◽  
Ali Goreyshi ◽  
Yadollah Omidi
Keyword(s):  
Colon Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Leuconostoc Mesenteroides ◽  
Colon Cancer Cells ◽  
Mapk Pathways

scholarly journals Restoration of Transforming Growth Factor-β Receptor II Expression in Colon Cancer Cells with Microsatellite Instability Increases Metastatic Potential in Vivo

2011 ◽  
Vol 286 (18) ◽  
pp. 16082-16090 ◽  
Author(s):  
Xiao-Qiong Liu ◽  
Ashwani Rajput ◽  
Liying Geng ◽  
Melanie Ongchin ◽  
Anathbandhu Chaudhuri ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Growth Factor ◽  
Microsatellite Instability ◽  
Cell Survival ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Tgfβ Signaling ◽  
Tgfβ Receptor

Microsatellite instability (MSI), which occurs in 15% of colorectal cancer, has been shown to have a lower incidence of metastasis and better patient survival rates compared with microsatellite stable colorectal cancer. However, a mechanistic understanding of the basis for this difference is very limited. Here, we show that restoration of TGFβ signaling by re-expression of TGFβ receptor II in MSI colon cancer cells increased PI3K/AKT activation, conferred resistance to growth factor deprivation stress-induced apoptosis, and promoted cell motility in vitro. Treatment with a potent PI3K inhibitor (LY294002) blocked the prosurvival and promotility effects of TGFβ, indicating that TGFβ-mediated promotion of cell survival and motility is dependent upon activation of the PI3K/AKT pathway. Analysis of apoptotic effectors that are affected by TGFβ signaling indicated that Bim is an effector of TGFβ-mediated survival. In addition, TGFβ-induced down-regulation of E-cadherin contributed to the prosurvival effect of TGFβ, and restoration of TGFβ signaling in MSI colon cancer cells increased liver metastasis in an orthotopic model in vivo. Taken together, our results demonstrate that restoration of TGFβ signaling promotes cell survival, motility, and metastatic progression in MSI colon cancer cells and indicate that TGFβ receptor II mutations contribute to the favorable outcomes in colon cancer patients with MSI.

Anticarcinogenic Effects of the Ethanolic Extract ofSalix aegyptiacain Colon Cancer Cells: Involvement of Akt/PKB and MAPK Pathways

2013 ◽  
Vol 65 (7) ◽  
pp. 1045-1058 ◽  
Author(s):  
Shabnam Enayat ◽  
Müşerref Şeyma Ceyhan ◽  
Arif Ahmet Başaran ◽  
Mayda Gürsel ◽  
Sreeparna Banerjee
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Ethanolic Extract ◽  
Colon Cancer Cells ◽  
Mapk Pathways

scholarly journals Reorganization of ErbB Family and Cell Survival Signaling after Knock-down of ErbB2 in Colon Cancer Cells

2005 ◽  
Vol 280 (29) ◽  
pp. 27383-27392 ◽  
Author(s):  
Yi Peter Hu ◽  
Srinivas Venkateswarlu ◽  
Natalia Sergina ◽  
Gillian Howell ◽  
Patricia St. Clair ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Erbb Family ◽  
Knock Down ◽  
Survival Signaling

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 TGFβ and IGF1R signaling activates protein kinase A through differential regulation of ezrin phosphorylation in colon cancer cells

2018 ◽  
Vol 293 (21) ◽  
pp. 8242-8254 ◽  
Author(s):  
Premila D. Leiphrakpam ◽  
Michael G. Brattain ◽  
Jennifer D. Black ◽  
Jing Wang
Keyword(s):  
Colon Cancer ◽  
Growth Factor ◽  
Protein Kinase ◽  
Cell Survival ◽  
Protein Kinase A ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Independent Manner ◽  
Igf1r Signaling ◽  
Kinase A

Aberrant cell survival plays a critical role in cancer progression and metastasis. We have previously shown that ezrin, a cAMP-dependent protein kinase A–anchoring protein (AKAP), is up-regulated in colorectal cancer (CRC) liver metastasis. Phosphorylation of ezrin at Thr-567 activates ezrin and plays an important role in CRC cell survival associated with XIAP and survivin up-regulation. In this study, we demonstrate that in FET and GEO colon cancer cells, knockdown of ezrin expression or inhibition of ezrin phosphorylation at Thr-567 increases apoptosis through protein kinase A (PKA) activation in a cAMP-independent manner. Transforming growth factor (TGF) β signaling inhibits ezrin phosphorylation in a Smad3-dependent and Smad2-independent manner and regulates pro-apoptotic function through ezrin-mediated PKA activation. On the other hand, ezrin phosphorylation at Thr-567 by insulin-like growth factor 1 receptor (IGF1R) signaling leads to cAMP-dependent PKA activation and enhances cell survival. Further studies indicate that phosphorylated ezrin forms a complex with PKA RII, and dephosphorylated ezrin dissociates from the complex and facilitates the association of PKA RII with AKAP149, both of which activate PKA yet lead to either cell survival or apoptosis. Thus, our studies reveal a novel mechanism of differential PKA activation mediated by TGFβ and IGF1R signaling through regulation of ezrin phosphorylation in CRC, resulting in different cell fates. This is of significance because TGFβ and IGF1R signaling pathways are well-characterized tumor suppressor and oncogenic pathways, respectively, with important roles in CRC tumorigenesis and metastasis. Our studies indicate that they cross-talk and antagonize each other's function through regulation of ezrin activation. Therefore, ezrin may be a potential therapeutic target in CRC.

scholarly journals Activation of Akt and MAPK pathways enhances the tumorigenicity of CD133+ primary colon cancer cells

2010 ◽  
Vol 31 (8) ◽  
pp. 1376-1380 ◽  
Author(s):  
Y. K. Wang ◽  
Y. L. Zhu ◽  
F. M. Qiu ◽  
T. Zhang ◽  
Z. G. Chen ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
Mapk Pathways ◽  
Primary Colon Cancer ◽  
Primary Colon
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