Yanan Cui’s research while affiliated with The Second Xiangya Hospital of Central South University and other places

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Publications (2)


Correction to: Ready player one? Autophagy shapes resistance to photodynamic therapy in cancers
  • Article
  • Publisher preview available

February 2019

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16 Reads

Apoptosis

Xian Duan

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Bo Chen

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Yanan Cui

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[...]

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The below funding information was not submitted and hence not included in the original publication. The funding information is given below. © 2018, Springer Science+Business Media, LLC, part of Springer Nature.

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PDT-induced autophagy and autophagy processes. The signalling pathways used by PDT to affect autophagy activation include the AMPK/mTOR, Akt/mTOR, and p53/AMPK/mTOR pathways. mTOR inhibition is critical to inducing autophagy; it leads to the dissociation of mTORC1 and results in the sequential activation of Atg13, UKL1/2, and FIP200. Other non-canonical pathways have also been detected in PDT-induced autophagy activation. PDT activates p38MAPK and increases the expression of the autophagy receptors p62 and NBR1. PDT promotes the transcription factor HIF-1α, thereby increasing the expression of VMP1 and activating VMP1-based autophagy. PDT also inhibits Akt activation and thus decreases the expression of the anti-apoptotic factor BCL2, resulting in an increase in Beclin1. Additionally, ER stress-based sensors, such as RNA-activated protein kinase (PKR)-like ER kinase (PERK) and activating transcription factor (ATF) 6, improve the expression of a series of autophagy-associated proteins, including Atg16L1, Atg12, Atg3, Beclin1, p62, Atg7, Atg10, and Atg5. The second step of the autophagy process is mediated by the class III P13K protein complex, which is responsible for vesicular nucleation and leads to the formation of phagophores. Third, the Atg12-Atg16L1-Atg5 conjugate increases the elongation of the phagophore. The conjugate consisting of phosphatidylethanolamine (PE) and microtubule-associated protein 1-light chain 3 (LC3) leads to LC3 lipidation and localization on autophagosome membranes. Then, the autophagosome is transferred to the lysosome via a microtubule-mediated mechanism and subsequently fuses with lysosomes for further degradation of its cargo
The mechanisms underlying the role of autophagy in resistance to PDT. PDT induces a marked increase in autophagy in cancer cells. Conversely, enhanced autophagy can promote resistance to PDT via the following potential mechanisms. a Autophagy degrades dysfunctional or impaired cellular components and organelles, provides energy and material for cells, and maintains cellular homeostasis. Cells with defective autophagy are susceptible to PDT, which leads to apoptosis. b Dynamic signalling interactions between cancer cells and their microenvironment can induce a transient, resistant state in the cancer cells. For example, high mobility group box1 (HMGB1) is secreted by endothelial cells and can confer cancer cells with resistance to apoptosis and pro-survival autophagy (Ref 99), whereas in cancer-associated fibroblasts, autophagy supports energy metabolism and the growth of neighbouring cancer cells. c Autophagy stimulates epithelial–mesenchymal transition (EMT), resulting in more mesenchymal stem-like phenotypes. Autophagy protects cells from anoikis when cells detach from the extracellular membrane (ECM). Autophagy also plays a direct role in regulating cell motility and invasion. Autophagy supports the disseminating cells with an energy supply and facilitates cancer cell dormancy
Ready player one? Autophagy shapes resistance to photodynamic therapy in cancers

December 2018

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130 Reads

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34 Citations

Apoptosis

Photodynamic therapy (PDT) is a procedure used in cancer therapy that has been shown to be useful for certain indications. Considerable evidence suggests that PDT might be superior to conventional modalities for some indications. In this report, we examine the relationship between PDT responsiveness and autophagy, which can exert a cytoprotective effect. Autophagy is an essential physiological process that maintains cellular homeostasis by degrading dysfunctional or impaired cellular components and organelles via a lysosome-based pathway. Autophagy, which includes macroautophagy and microautophagy, can be a factor that decreases or abolishes responses to various therapeutic protocols. We systematically discuss the mechanisms underlying cell-fate decisions elicited by PDT; analyse the principles of PDT-induced autophagy, macroautophagy and microautophagy; and present evidence to support the notion that autophagy is a critical mechanism in resistance to PDT. A combined strategy involving autophagy inhibitors may be able to further enhance PDT efficacy. Finally, we provide suggestions for future studies, note where our understanding of the relevant molecular regulators is deficient, and discuss the correlations among PDT-induced resistance and autophagy, especially microautophagy.

Citations (1)


... During the process of PDT, cells under stress induce autophagy to recycle valuable resources to fight against cytotoxic stress. 114 Taking melanoma as an example, Valli et al. reported that autophagy could prevent cells from undergoing apoptosis by regulating the phototoxicity of PSs and the cleavage of PARP-1 ( Figure 6A). 60 Moreover, cell-protective autophagy may also be responsible for PDT resistance. ...

Reference:

Cell death: The underlying mechanisms of photodynamic therapy for skin diseases
Ready player one? Autophagy shapes resistance to photodynamic therapy in cancers

Apoptosis