scholarly journals A novel double-negative feedback loop between miR-489 and the HER2-SHP2-MAPK signaling axis regulates breast cancer cell proliferation and tumor growth

Oncotarget ◽  
2016 ◽  
Vol 7 (14) ◽  
pp. 18295-18308 ◽  
Author(s):  
Yogin Patel ◽  
Nirav Shah ◽  
Ji Shin Lee ◽  
Eleni Markoutsa ◽  
Chunfa Jie ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Mapk Signaling ◽  
Negative Feedback Loop ◽  
Double Negative ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Signaling Axis

scholarly journals HIC1 and miR-23~27~24 clusters form a double-negative feedback loop in breast cancer

2016 ◽  
Vol 24 (3) ◽  
pp. 421-432 ◽  
Author(s):  
Yanbo Wang ◽  
Hongwei Liang ◽  
Geyu Zhou ◽  
Xiuting Hu ◽  
Zhengya Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Double Negative

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.

scholarly journals AMPK–Akt Double-Negative Feedback Loop in Breast Cancer Cells Regulates Their Adaptation to Matrix Deprivation

2018 ◽  
Vol 78 (6) ◽  
pp. 1497-1510 ◽  
Author(s):  
Manipa Saha ◽  
Saurav Kumar ◽  
Shoiab Bukhari ◽  
Sai A. Balaji ◽  
Prashant Kumar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Negative Feedback ◽  
Breast Cancer Cells ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Double Negative

scholarly journals miR-30a/SOX4 Double Negative Feedback Loop is modulated by Disulfiram and regulates EMT and Stem Cell-like properties in Breast Cancer

2021 ◽  
Vol 12 (16) ◽  
pp. 5053-5065
Author(s):  
Zijian Liu ◽  
Mi Mi ◽  
Xin Zheng ◽  
Caijiao Zhang ◽  
Fang Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Double Negative

scholarly journals Multi-Stability and Consequent Phenotypic Plasticity in AMPK-Akt Double Negative Feedback Loop in Cancer Cells

2021 ◽  
Vol 10 (3) ◽  
pp. 472
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 ◽  
The Cancer Genome Atlas ◽  
Phenotypic Switching ◽  
Negative Feedback Loop ◽  
Double Negative

Adaptation 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 (AMP-activated protein kinase) and Akt can regulate the adaptation of breast cancer cells to matrix-deprivation stress. This feedback loop can significantly generate 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 The Cancer Genome Atlas (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 multi-stability and drive phenotypic switching and heterogeneity in a cancer cell population.

scholarly journals Interrupted E2F1-miR-34c-SCF negative feedback loop by hyper-methylation promotes colorectal cancer cell proliferation

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Shu Yang ◽  
Bo Wu ◽  
Haimei Sun ◽  
Fengqing Ji ◽  
Tingyi Sun ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Cancer Cell ◽  
Negative Feedback ◽  
Stem Cell Factor ◽  
Feedback Loop ◽  
Colorectal Cancer Cell ◽  
Negative Feedback Loop ◽  
Cancer Cell Proliferation

E2F1 promoted miR-34c transcription which reduced its target stem cell factor (SCF) and inhibited colorectal cancer (CRC) cell proliferation. While, SCF increased E2F1 production, suggesting an existence of E2F1-miR-34c-SCF negative feedback loop, which was interrupted by hyper-methylation of miR-34c promoter in CRC cells.

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