scholarly journals MicroRNA-22 suppresses the growth, migration and invasion of colorectal cancer cells through a Sp1 negative feedback loop

Oncotarget ◽  
2017 ◽  
Vol 8 (22) ◽  
pp. 36266-36278 ◽  
Author(s):  
Shu-Sen Xia ◽  
Guang-Jun Zhang ◽  
Zuo-Liang Liu ◽  
Hong-Peng Tian ◽  
Yi He ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Migration And Invasion ◽  
Negative Feedback Loop ◽  
Colorectal Cancer Cells

scholarly journals A Negative Feedback Loop Between NAMPT and TGF-β Signaling Pathway in Colorectal Cancer Cells

2021 ◽  
Vol Volume 14 ◽  
pp. 187-198
Author(s):  
Xiaoqun Lv ◽  
Jinguo Zhang ◽  
Jun Zhang ◽  
Wencai Guan ◽  
Weifang Ren ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Colorectal Cancer Cells

scholarly journals Pals1 prevents Rac1-dependent colorectal cancer cell metastasis by inhibiting Arf6

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Simona Mareike Lüttgenau ◽  
Christin Emming ◽  
Thomas Wagner ◽  
Julia Harms ◽  
Justine Guske ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Scaffolding Protein ◽  
Migration And Invasion ◽  
Tight Junction Formation ◽  
Cell Metastasis ◽  
Colorectal Cancer Cells

AbstractLoss of apical-basal polarity and downregulation of cell-cell contacts is a critical step during the pathogenesis of cancer. Both processes are regulated by the scaffolding protein Pals1, however, it is unclear whether the expression of Pals1 is affected in cancer cells and whether Pals1 is implicated in the pathogenesis of the disease.Using mRNA expression data and immunostainings of cancer specimen, we show that Pals1 is frequently downregulated in colorectal cancer, correlating with poorer survival of patients. We further found that Pals1 prevents cancer cell metastasis by controlling Rac1-dependent cell migration through inhibition of Arf6, which is independent of the canonical binding partners of Pals1. Loss of Pals1 in colorectal cancer cells results in increased Arf6 and Rac1 activity, enhanced cell migration and invasion in vitro and increased metastasis of transplanted tumor cells in mice. Thus, our data reveal a new function of Pals1 as a key inhibitor of cell migration and metastasis of colorectal cancer cells. Notably, this new function is independent of the known role of Pals1 in tight junction formation and apical-basal polarity.

LncRNA FTX Promotes Colorectal Cancer Cells Migration and Invasion by miRNA-590-5p/RBPJ Axis

2021 ◽  
Author(s):  
Guo-Qun Chen ◽  
Zhi-Ming Liao ◽  
Jiao Liu ◽  
Fang Li ◽  
Da Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Colorectal Cancer Cells

scholarly journals Upregulation of microRNA-155 promotes the migration and invasion of colorectal cancer cells through the regulation of claudin-1 expression

2013 ◽  
Vol 31 (6) ◽  
pp. 1375-1380 ◽  
Author(s):  
GUANG-JUN ZHANG ◽  
HUA-XU XIAO ◽  
HONG-PENG TIAN ◽  
ZUO-LIANG LIU ◽  
SHU-SEN XIA ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Colorectal Cancer Cells

scholarly journals RasGRF2 promotes migration and invasion of colorectal cancer cells by modulating expression of MMP9 through Src/Akt/NF-κB pathway

2018 ◽  
Vol 20 (4) ◽  
pp. 435-443 ◽  
Author(s):  
Peifen Lu ◽  
Junjun Chen ◽  
Lihong Yan ◽  
Lijun Yang ◽  
Litao Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Colorectal Cancer Cells

scholarly journals Multistability and consequent phenotypic plasticity in AMPK-Akt double negative feedback loop in cancer cells

2020 ◽  
Author(s):  
Adithya Chedere ◽  
Kishore Hari ◽  
Saurav Kumar ◽  
Annapoorni Rangarajan ◽  
Mohit Kumar Jolly
Keyword(s):  
Breast Cancer ◽  
Phenotypic Plasticity ◽  
Cancer Cells ◽  
Cell Population ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Phenotypic Switching ◽  
Negative Feedback Loop ◽  
Double Negative ◽  
Protein Levels

AbstractAdaptation and survival of cancer cells to various stress and growth factor conditions is crucial for successful metastasis. A double-negative feedback loop between two serine/threonine kinases AMPK and Akt can regulate the adaptation of breast cancer cells to matrix-deprivation stress. This feedback loop can generate majorly two phenotypes or cell states: matrix detachment-triggered pAMPKhigh/ pAktlow state, and matrix (re)attachment-triggered pAkthigh/ pAMPKlow state. However, whether these two cell states can exhibit phenotypic plasticity and heterogeneity in a given cell population, i.e., whether they can co-exist and undergo spontaneous switching to generate the other subpopulation, remains unclear. Here, we develop a mechanism-based mathematical model that captures the set of experimentally reported interactions among AMPK and Akt. Our simulations suggest that the AMPK-Akt feedback loop can give rise to two co-existing phenotypes (pAkthigh/ pAMPKlow and pAMPKhigh/pAktlow) in specific parameter regimes. Next, to test the model predictions, we segregated these two subpopulations in MDA-MB-231 cells and observed that each of them was capable of switching to another in adherent conditions. Finally, the predicted trends are supported by clinical data analysis of TCGA breast cancer and pan-cancer cohorts that revealed negatively correlated pAMPK and pAkt protein levels. Overall, our integrated computational-experimental approach unravels that AMPK-Akt feedback loop can generate multistability and drive phenotypic switching and heterogeneity in a cancer cell population.

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