scholarly journals YAP regulates ALDH1A1 expression and stem cell property of bladder cancer cells

2018 ◽  
Vol Volume 11 ◽  
pp. 6657-6663 ◽  
Author(s):  
Aiyue Zhao ◽  
Yijun Dai ◽  
Jianfeng Lian ◽  
Yan Huang ◽  
Jianguang Lin ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Stem Cell ◽  
Cancer Cells ◽  
Stem Cell Property ◽  
Bladder Cancer Cells ◽  
Cell Property

scholarly journals CCL21 Facilitates Chemoresistance and Cancer Stem Cell-Like Properties of Colorectal Cancer Cells through AKT/GSK-3β/Snail Signals

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Lin-Lin Lu ◽  
Xiao-Hui Chen ◽  
Ge Zhang ◽  
Zong-Cai Liu ◽  
Nong Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Mrna Levels ◽  
Stem Cell Property ◽  
Mammosphere Formation ◽  
Cell Property ◽  
Gsk 3Β ◽  
Hct116 Cells

Some evidence indicated that chemoresistance associates with the acquisition of cancer stem-like properties. Recent studies suggested that chemokines can promote the chemoresistance and stem cell properties in various cancer cells, while the underling mechanism is still not completely illustrated. In our study, we found that CCL21 can upregulate the expression of P-glycoprotein (P-gp) and stem cell property markers such as Bmi-1, Nanog, and OCT-4 in colorectal cancer (CRC) HCT116 cells and then improve the cell survival rate and mammosphere formation. Our results suggested that Snail was crucial for CCL21-mediated chemoresistance and cancer stem cell property in CRC cells. Further, we observed that CCL21 treatment increased the protein but not mRNA levels of Snail, which suggested that CCL21 upregulates Snail via posttranscriptional ways. The downstream signals AKT/GSK-3βmediated CCL21 induced the upregulation of Snail due to the fact that CCL21 treatment can obviously phosphorylate both AKT and GSK-3β. The inhibitor of PI3K/Akt, LY294002 significantly abolished CCL21 induced chemoresistance and mammosphere formation of HCT116 cells. Collectively, our results in the present study revealed that CCL21 can facilitate chemoresistance and stem cell property of CRC cells via the upregulation of P-gp, Bmi-1, Nanog, and OCT-4 through AKT/GSK-3β/Snail signals, which suggested a potential therapeutic approach to CRC patients.

scholarly journals The FBXW2–MSX2–SOX2 axis regulates stem cell property and drug resistance of cancer cells

2019 ◽  
Vol 116 (41) ◽  
pp. 20528-20538 ◽  
Author(s):  
Yuan Yin ◽  
Chuan-Ming Xie ◽  
Hua Li ◽  
Mingjia Tan ◽  
Guoan Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Stem Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
E3 Ligase ◽  
Stem Cell Property ◽  
Sox2 Expression ◽  
Cell Property

SOX2 is a key transcription factor that plays critical roles in maintaining stem cell property and conferring drug resistance. However, the underlying mechanisms by which SOX2 level is precisely regulated remain elusive. Here we report that MLN4924, also known as pevonedistat, a small-molecule inhibitor of neddylation currently in phase II clinical trials, down-regulates SOX2 expression via causing accumulation of MSX2, a known transcription repressor of SOX2 expression. Mechanistic characterization revealed that MSX2 is a substrate of FBXW2 E3 ligase. FBXW2 binds to MSX2 and promotes MSX2 ubiquitylation and degradation. Likewise, FBXW2 overexpression shortens the protein half-life of MSX2, whereas FBXW2 knockdown extends it. We further identified hypoxia as a stress condition that induces VRK2 kinase to facilitate MSX2–FBXW2 binding and FBXW2-mediated MSX2 ubiquitylation and degradation, leading to SOX2 induction via derepression. Biologically, expression of FBXW2 or SOX2 promotes tumor sphere formation, which is blocked by MSX2 expression. By down-regulating SOX2 through inactivation of FBXW2 E3 ligase, MLN4924 sensitizes breast cancer cells to tamoxifen in both in vitro and in vivo cancer cell models. Thus, a negative cascade of the FBXW2–MSX2–SOX2 axis was established, which regulates stem cell property and drug resistance. Finally, an inverse correlation of expression was found between FBXW2 and MSX2 in lung and breast cancer tissues. Collectively, our study revealed an anticancer mechanism of MLN4924. By inactivating FBXW2, MLN4924 caused MSX2 accumulation to repress SOX2 expression, leading to suppression of stem cell property and sensitization of breast cancer cells to tamoxifen.

758: Inflammatory and Anti-Inflammatory Regulators alter Levels of an Inhibitor of Apoptosis (IAP), Survivin, in T-24 Bladder Cancer Cells

2007 ◽  
Vol 177 (4S) ◽  
pp. 254-254
Author(s):  
Justin J. Cohen ◽  
Bayan T. Takizawa ◽  
Hristos Z. Kaimkliotis ◽  
David J. Rosenberg ◽  
Marcia A. Wheeler ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Inhibitor Of Apoptosis ◽  
Bladder Cancer Cells ◽  
Anti Inflammatory

792: Role of Oxidative Stress in Tumorigenic Potential of Bladder Cancer Cells

2005 ◽  
Vol 173 (4S) ◽  
pp. 214-215 ◽  
Author(s):  
Daniel Cho ◽  
Xiao Fang Ha ◽  
J. Andre Melendez ◽  
Louis J. Giorgi ◽  
Badar M. Mian
Keyword(s):  
Oxidative Stress ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Tumorigenic Potential ◽  
Bladder Cancer Cells

627: Multitarget Gene Inhibition by Synthetic Nucleic Acids in Bladder Cancer Cells

2006 ◽  
Vol 175 (4S) ◽  
pp. 202-202 ◽  
Author(s):  
Yvonne Burmeister ◽  
Kai Kraemer ◽  
Susanne Fuessel ◽  
Matthias Kotzsch ◽  
Axel Meye ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Nucleic Acids ◽  
Cancer Cells ◽  
Bladder Cancer Cells ◽  
Gene Inhibition

723: Chemokine Receptor CXCR4 Mediates Migration and Invasion of Bladder Cancer Cells

2004 ◽  
Vol 171 (4S) ◽  
pp. 192-192 ◽  
Author(s):  
Margitta Retz ◽  
Sukhvinder S. Sidhu ◽  
Gregory M. Dolganov ◽  
Jan Lehmann ◽  
Peter R. Carroll ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Chemokine Receptor ◽  
Migration And Invasion ◽  
Chemokine Receptor Cxcr4 ◽  
Bladder Cancer Cells
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