Frontiers | Emerging roles of endoplasmic reticulum stress in the cellular plasticity of cancer cells
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ER stress induces the expression of cyclase-associated protein 2 (CAP2) and promotes EMT via the activation of Rac1 and ERK in liver cancer cells urthermore, CSCs exhibit epigenetic plasticity and therapeutic resistance, which contribute to cancer progression or relapse. Recent evidence also suggest
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- ER stress induces the expression of cyclase-associated protein 2 (CAP2) and promotes EMT via the activation of Rac1 and ERK in liver cancer cells
- urthermore, CSCs exhibit epigenetic plasticity and therapeutic resistance, which contribute to cancer progression or relapse. Recent evidence also suggests that drug-resistant cells possess abnormal energetic and metabolic pathways that are involved in the induction, maintenance, and alteration of multidrug resistance (MDR) phenotype
- Cells expressing CSC-associated markers in glioblastoma do not represent a clonal entity but rather a plastic state that most cancer cells can adapt in response to microenvironmental signals
- CSCs can enter a dormant cellular state and exist in the G0 phase, which makes them resistant to conventional therapies that target actively dividing cells. Quiescence can be induced by altered microenvironmental cues or drug treatments. Breast cancer disseminated tumor cells (BC DTCs) may be instructed to enter dormancy by bone marrow NG2+/Nestin+
- hronic ER stress promotes immunosuppressive phenotypes of immune cells in various diseases, such as cancer and inflammation
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