scholarly journals Dynamic modelling of oestrogen signalling and cell fate in breast cancer cells

2011 ◽  
Vol 11 (7) ◽  
pp. 523-532 ◽  
Author(s):  
John J. Tyson ◽  
William T. Baumann ◽  
Chun Chen ◽  
Anael Verdugo ◽  
Iman Tavassoly ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Fate ◽  
Breast Cancer Cells ◽  
Dynamic Modelling ◽  
Oestrogen Signalling

scholarly journals HER2-Targeted Tyrosine Kinase Inhibitors Cause Therapy-Induced-Senescence in Breast Cancer Cells

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 197 ◽  
Author(s):  
Martina S.J. McDermott ◽  
Neil Conlon ◽  
Brigid C. Browne ◽  
Adam Szabo ◽  
Naoise C. Synnott ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tyrosine Kinase ◽  
Cancer Cells ◽  
Tyrosine Kinase Inhibitors ◽  
Cell Fate ◽  
Breast Cancer Cells ◽  
Kinase Inhibitors ◽  
Single Agent ◽  
Prolonged Treatment ◽  
Her2 Positive

Prolonged treatment of HER2 positive breast cancer cells with tyrosine kinase inhibitors (TKIs) leads to the emergence of acquired resistance. However, the effects of continuous TKI exposure on cell fate, and the steps leading to the acquisition of a resistant phenotype are poorly understood. To explore this, we exposed five HER2 positive cells lines to HER2 targeted therapies for periods of up to 4 weeks and examined senescence associated β-galactosidase (SA-β-gal) activity together with additional markers of senescence. We found that lapatinib treatment resulted in phenotypic alterations consistent with a senescent phenotype and strong SA-β-gal activity in HER2-positive cell lines. Lapatinib-induced senescence was associated with elevated levels of p15 and p27 but was not dependent on the expression of p16 or p21. Restoring wild type p53 activity either by transfection or by treatment with APR-246, a molecule which reactivates mutant p53, blocked lapatinib-induced senescence and caused increased cell death. In contrast to lapatinib, SA-β-gal activity was not induced by exposing the cells to trastuzumab as a single agent but co-administration of lapatinib and trastuzumab induced senescence, as did treatment of the cells with the irreversible HER2 TKIs neratinib and afatinib. Neratinib- and afatinib-induced senescence was not reversed by removing the drug whereas lapatinib-induced senescence was reversible. In summary, therapy-induced senescence represents a novel mechanism of action of HER2 targeting agents and may be a potential pathway for the emergence of resistance.

scholarly journals A-kinase anchoring protein BIG3 coordinates oestrogen signalling in breast cancer cells

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Tetsuro Yoshimaru ◽  
Masaya Ono ◽  
Yoshimi Bando ◽  
Yi-An Chen ◽  
Kenji Mizuguchi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Anchoring Protein ◽  
Oestrogen Signalling

scholarly journals Role of sphingolipids in oestrogen signalling in breast cancer cells: an update

2013 ◽  
Vol 220 (3) ◽  
pp. R25-R35 ◽  
Author(s):  
O Sukocheva ◽  
C Wadham
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Second Messengers ◽  
Membrane Receptors ◽  
Future Research ◽  
Specific Effects ◽  
Oestrogen Signalling ◽  
Signalling Cascade

The signaling pathways activated by the steroid hormone oestrogen include a variety of cytoplasmic second messengers linked to a multitude of tissue-specific effects. In the last decade, sphingolipids and their membrane receptors were added to the list of oestrogen-activated mediators. Oestrogen triggers the sphingolipid signalling cascade in various tissues including breast cancer. Extensive research has shown that sphingolipids are the key regulatory molecules in growth factor networks. Sphingolipids can control the rate of cell proliferation and the differentiation outcome during malignant transformation. In this study, we summarise novel experimental evidences linking sphingolipids to oestrogen-activated effects, highlight the role of sphingolipids in cancer cells and discuss new avenues for future research at the intersection between oestrogen and sphingolipid signalling.

HPIP protooncogene differentially regulates metabolic adaptation and cell fate in breast cancer cells under glucose stress via AMPK and RNF2 dependent pathways

2021 ◽  
Author(s):  
Vasudevarao Penugurti ◽  
Saratchandra Singh Khumukcham ◽  
Chiranjeevi Padala ◽  
Anju Dwivedi ◽  
Karthik Reddy Kamireddy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Fate ◽  
Breast Cancer Cells ◽  
Metabolic Adaptation

scholarly journals BCL2 and CASP8 regulation by NF‐κB differentially affect mitochondrial function and cell fate in antiestrogen‐sensitive and ‐resistant breast cancer cells

2010 ◽  
Vol 24 (6) ◽  
pp. 2040-2055 ◽  
Author(s):  
Ruchi Nehra ◽  
Rebecca B. Riggins ◽  
Ayesha N. Shajahan ◽  
Alan Zwart ◽  
Anatasha C. Crawford ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Fate ◽  
Mitochondrial Function ◽  
Breast Cancer Cells
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