The crosstalk between classic cell signaling pathways, non-coding RNAs and ferroptosis in drug resistance of tumors
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Autophagy and apoptosis are catabolic pathways essential for organismal homeostasis. Autophagy is normally a cell-survival pathway involving the degradation and recycling of obsolete, damaged, or harmful macromolecular assemblies; however, excess autophagy has been implicated in type II cell death. Apoptosis is the canonical programmed cell death pathway. Autophagy and apoptosis have now been shown to be interconnected by several molecular nodes of crosstalk, enabling the coordinate regulation of degradation by these pathways. Normally, autophagy and apoptosis are both tumor suppressor pathways. Autophagy fulfils this role as it facilitates the degradation of oncogenic molecules, preventing development of cancers, while apoptosis prevents the survival of cancer cells. Consequently, defective or inadequate levels of either autophagy or apoptosis can lead to cancer. However, autophagy appears to have a dual role in cancer, as it has now been shown that autophagy also facilitates the survival of tumor cells in stress conditions such as hypoxic or low-nutrition environments. Here we review the multiple molecular mechanisms of coordination of autophagy and apoptosis and the role of the proteins involved in this crosstalk in cancer. A comprehensive understanding of the interconnectivity of autophagy and apoptosis is essential for the development of effective cancer therapeutics.
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Autophagy is also known as programmed type Ⅱ cell death. And autophagy has been shown to contribute to the occurrence and development of many diseases. More and more studies have suggested that the molecular regulation of autophagy and apoptosis pathways are inter-connected——numerous death stimuli are capable of activating either pathway, and both pathways share several genes, they can even transform with each other. A comprehensive study of the crosstalk between autophagy and apoptosis will bring a breakthrough on the cognition of the treatment of cancer and other diseases.
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Autophagy is a degradation mechanism involved in quality and quantity control of cytoplasmic proteins and organelles,regarded as a programmed cell death juxtaposed with apoptosis and necrosis.Unravelled correlations between autophagy,apoptosis and necrosis,however,suggest that autophagy may be a manager of programme cell death,and determine whether cell death occurs and selection of death pathways in response to stress.Revealing molecular mechanism of autophagy contributes to understand these seemingly contradictory views.Elucidation of autophagy′s role in programmed cell death has important practical significance for treating tumor.
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This chapter contains sections titled: Introduction Types of Programmed Cell Death Type 1 Programmed Cell Death Type 2 Programmed Cell Death Type 3 Programmed Cell Death Other Types of Programmed Cell Death The Contribution of Autophagy to Programmed Cell Death Death Processes That Require atg Genes The Combined Activation of Autophagy and Apoptosis during Programmed Cell Death Emerging Relationships between Apoptosis and Autophagy Autophagy and Cell Survival Autophagy is Cytoprotective during Nutrient Depletion in Mammalian Cells Autophagy and Neuroprotection Cytoprotective Roles of Autophagy in the Response to Infectious Pathogens Autophagy and Organism Survival Concluding Remarks Acknowledgments References
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Autophagy and apoptosis play important roles in the development, cellular homeostasis and, especially, oncogenesis of mammals. They may be triggered by common upstream signals, resulting in combined autophagy and apoptosis. In other instances, they may be mutually exclusive. Recent studies have suggested possible molecular mechanisms for crosstalk between autophagy and apoptosis. Bcl-2 and Bcl-xL, the well-characterized apoptosis guards, appear to be important factors in autophagy, inhibiting Beclin 1-mediated autophagy by binding to Beclin 1. In addition, Beclin 1, Bcl-2 and Bcl-xL can cooperate with Atg5 or Ca(2+) to regulate both autophagy and apoptosis. Thus, Bcl-2 and Bcl-xL represent a molecular link between autophagy and apoptosis. Here, we discuss the possible roles of Bcl-2 and Bcl-xL in apoptosis and autophagy, and the crosstalk between them.
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The relations between reactive oxygen species(ROS)and autophagy is complex.ROS as a signaling molecule is involved not only in the cell proliferation and differentiation,but also in the formation of intracellular autophagy.Here is to make a review on the molecullar mechanism of ROS-mediated autophagy,and the roles of ROS and autophagy in the ischemia-reperfusion injury,tumor and infection,so as to provide new strategies for the treatment of related diseases.
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