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Under normal circumstances, autophagy is typically activated in cells under stress conditions, thereby maintaining the survival of cancer cells. However, sometimes, continued and heightened stress leads to autophagy overactivated and causes cell damage, leading to cell death. However, the regulation of autophagy by stress responses is not unidirectional; autophagy can also control cellular stress responses by modulating ROS. In a word, they interact with each other, jointly regulating the survival and death of cancer cells.
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Autophagy is a conservative catabolic process that typically serves a cell‐protective function. Under stress conditions, when the cellular environment becomes unstable, autophagy is activated as an adaptive response for self‐protection. Autophagy delivers damaged cellular components to lysosomes for degradation and recycling, thereby providing esse...
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Citations
... This inhibition results in mTORC1 activation, which inhibits autophagy by phosphorylating ULK1, hence obstructing autophagosome formation [16]. In contrast, under stress circumstances, such as food restriction or hypoxia, PI3K/AKT signaling is suppressed, resulting in mTORC1 inhibition, which activates ULK1 and initiates autophagy [17]. This transition allows cells to decompose and reutilize intracellular constituents to sustain energy equilibrium and viability. ...
The phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) pathway plays a crucial role in the regulation of autophagy, a cellular mechanism vital for homeostasis through the degradation of damaged organelles and proteins. The dysregulation of this pathway is significantly associated with cancer progression, metastasis, and resistance to therapy. Targeting the PI3K/AKT/mTOR signaling pathway presents a promising strategy for cancer treatment; however, traditional therapeutics frequently encounter issues related to nonspecific distribution and systemic toxicity. Nanoparticle-based drug delivery systems represent a significant advancement in addressing these limitations. Nanoparticles enhance the bioavailability, stability, and targeted delivery of therapeutic agents, facilitating the precise modulation of autophagy in cancer cells. Functionalized nanoparticles, such as liposomes, polymeric nanoparticles, and metal-based nanocarriers, facilitate targeted drug delivery to tumor tissues, minimizing off-target effects and improving therapeutic efficacy. These systems can deliver multiple agents concurrently, enhancing the modulation of PI3K/AKT/mTOR-mediated autophagy and related oncogenic pathways. This review examines advancements in nanoparticle-mediated drug delivery that target the PI3K/AKT/mTOR pathway, emphasizing their contribution to improving precision and minimizing side effects in cancer therapy. The integration of nanotechnology with molecularly targeted therapies presents substantial potential for addressing drug resistance. Future initiatives must prioritize the optimization of these systems to enhance clinical translation and patient outcomes.
