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 ◽  
...  
Oncotarget ◽  
2017 ◽  
Vol 8 (22) ◽  
pp. 36266-36278 ◽  
Author(s):  
Shu-Sen Xia ◽  
Guang-Jun Zhang ◽  
Zuo-Liang Liu ◽  
Hong-Peng Tian ◽  
Yi He ◽  
...  

2021 ◽  
Vol 21 (4) ◽  
Author(s):  
Dan Yu ◽  
Haiping Liu ◽  
Jianli Qin ◽  
Mengjie Huangfu ◽  
Xiao Guan ◽  
...  

2021 ◽  
Vol 12 (6) ◽  
pp. 1678-1686
Author(s):  
Wei Zhang ◽  
Gang Wu ◽  
Peichun Sun ◽  
Yuanzeng Zhu ◽  
Han Zhang

2020 ◽  
Author(s):  
Adithya Chedere ◽  
Kishore Hari ◽  
Saurav Kumar ◽  
Annapoorni Rangarajan ◽  
Mohit Kumar Jolly

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.


2014 ◽  
Vol 26 (11) ◽  
pp. 2333-2342 ◽  
Author(s):  
Hung-Chih Hsu ◽  
Yi-Shiuan Liu ◽  
Kai-Chi Tseng ◽  
Bertrand Chin-Ming Tan ◽  
Shu-Jen Chen ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Wanjuan Xue ◽  
Yongcheng Liu ◽  
Ningning Xin ◽  
Jiyu Miao ◽  
Juan Du ◽  
...  

The study is aimed at investigating the role of Nei endonuclease VIII-like1 (NEIL1) in the pathogenesis of colorectal cancer (CRC). The human CRC (HCT116 and SW480) cells were subjected to the siRNA silencing and recombinant plasmid overexpression of NEIL1. Transfection of siNEIL1 significantly inhibited the cell growth. It also increased the Bax expression levels, while it decreased the Bcl-2 expression levels in human CRC cells, leading the Bax/Bcl-2 balance toward apoptosis. Moreover, the apoptosis was promoted through the caspase-9 signaling pathway. One the other hand, high expression of NEIL1 promoted the cell viability and reduced the apoptosis, inducing the balance of Bax/Bcl-2 in the human colon cancer cells to be antiapoptotic. In addition, the caspase-9 signaling pathway inhibited apoptosis, contrary to the results obtained by downregulating NEIL1 expression. Furthermore, NEIL1 was negatively regulated by miR-7-5p, indicating that miR-7-5p inhibited the NEIL1 expression after transcription. Overexpression of miR-7-5p reversed the effects of NEIL1 on these CRC cells. In conclusion, NEIL1 promotes the proliferation of CRC cells, which is regulated negatively by miR-7-5p. These findings suggest that NEIL1 is a potential therapeutic target for CRC.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Zhao Yang ◽  
Shengwu Liu ◽  
Mingao Zhu ◽  
Hong Zhang ◽  
Ji Wang ◽  
...  

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