p8 attenuates the apoptosis induced by dihydroartemisinin in cancer cells through promoting autophagy

Chen, Sang-Sang; Hu, Wei; Zeng, Wang; Lou, Xiang Yang; Zhou, Huijun

doi:10.1080/15384047.2015.1026477

Cited by 37 publications

(28 citation statements)

References 35 publications

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“…Consistent with our results, autophagy was also activated by DHA in myeloma cancer and glioma cells2028. In the HeLa and HCT116 cells, DHA induced autophagy by upregulating the level of stress-regulated protein p8, and the activation of autophagy attenuated the DHA-induced apoptosis adaptively29. In the ovarian cancer cells, autophagy was also activated by DHA via the mTOR pathway, although the association between apoptosis and autophagy was not proven30.…”

Section: Discussionsupporting

confidence: 79%

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Jiang

Meng

Lee

et al. 2016

Sci Rep

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Osteoarthritis is a disease with inflammatory and catabolic imbalance in cartilage. Dihydroartemisinin (DHA), a natural and safe anti-malarial agent, has been reported to inhibit inflammation, but its effects on chondrocytes have yet to be elucidated. We investigated the effects of DHA on catabolism in chondrocytes. Viability of SD rats chondrocytes was analyzed. Autophagy levels were determined via expression of autophagic markers LC3 and ATG5, GFP-LC3 analysis, acridine orange staining, and electron microscopy. ATG5 siRNA induced autophagic inhibition. Catabolic gene and chemokine expression was evaluated using qPCR. The NF-κB inhibitor SM7368 and p65 over-expression were used to analyze the role of NF-κB pathway in autophagic activation. A concentration of 1 μM DHA without cytotoxicity increased LC3-II and ATG5 levels as well as autophagosomal numbers in chondrocytes. DHA inhibited TNF-α-induced expression of MMP-3 and -9, ADAMTS5, CCL-2 and -5, and CXCL1, which was reversed by autophagic inhibition. TNF-α-stimulated nuclear translocation and degradation of the p65 and IκBα proteins, respectively, were attenuated in DHA-treated chondrocytes. NF-κB inhibition activated autophagy in TNF-α-treated chondrocytes, but p65 over-expression reduced the autophagic response to DHA. These results indicate that DHA might suppress the levels of catabolic and inflammatory factors in chondrocytes by promoting autophagy via NF-κB pathway inhibition.

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Section: Discussionsupporting

confidence: 79%

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Jiang

Meng

Lee

et al. 2016

Sci Rep

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“…In contrast, CQ pretreatment was shown to synergistically enhance artemisinin‐induced cell death in nonsmall cell lung cancer (NSCLC) A549 cells, suggesting that the timing of autophagy inhibition could affect the cellular context and response to artemisinin . The protective effect of autophagy following artemisinin treatment was shown more clearly by Chen et al., who identified the stress‐related protein p8 to be upregulated following artemisinin exposure in HeLa and HCT116 . The protein p8, in combination with ER stress‐related proteins ATF4 and CHOP, was shown to contribute to artemisinin‐induced autophagy.…”

Section: Artemisinin‐induced Cell Death and Related Mechanismsmentioning

confidence: 99%

Artemisinin as an anticancer drug: Recent advances in target profiling and mechanisms of action

Wong

Kalesh

et al. 2017

Medicinal Research Reviews

195

139

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“…Autophagy was investigated using supravital staining with AO, with a method that is wellknown in the literature [Paglin et al, 2001;Kanzawa et al, 2003;Chen et al, 2015;Li et al, 2015]. Depending on the acidity, AO stains the autophagosomes, the hallmark of autophagic process, from orange to red.…”

Section: Osteoblast Cell Morphology Correlates With Autophagy Inductionmentioning

confidence: 99%

A Key Role of Autophagy in Osteoblast Differentiation on Titanium-Based Dental Implants

Kaluđerović

Mojić

Schreckenbach³

et al. 2014

Cells Tissues Organs

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Autophagy plays an important role in embryogenesis, for the maintenance of tissue homeostasis and the elimination of damaged subcellular structures. Furthermore, autophagy could be a mode of physiological cell death and also be implicated in cell differentiation. Thus, we hypothesized that autophagy may have an impact on the differentiation of osteoblast cells influenced by various titanium-based surfaces. Interactions between smooth, commercially available pure titanium (Ti cp), rough Ticer, acid-etched Ti cp (SS) and M1-M3 (comprised of the monoclinic phase of sodium-titanium oxides and rutile; M2 contains amorphous calcium phosphates) and human osteoblast cells were investigated. Immunofluorescent staining was used for detecting autophagy, cell cluster formation and collagen type I (Col-1) expression. Flow cytometry was employed to identify autophagy, the production of endogenous nitric oxide (NO) and the size and granularity of the cells. Rough surfaces caused osteoblast differentiation via the autophagic-dependent PI3/Akt signalling pathway. These surfaces induced the formation of discrete populations of large, granular cells, i.e. mature osteoblasts. In addition, M1-M3 provoked the development of a third population of small, granular cells, responsible for cell cluster formation, which are important for the formation of bone noduli and mineralisation. The same surfaces induced faster osteoblast maturation and enhanced NO production, a hallmark of the already mentioned processes. Neither the mature osteoblasts nor the small cells appeared after the inhibition of autophagy. Inhibition of autophagy also prevented cell cluster formation. We demonstrate that autophagy plays an essential role in the osteoblast differentiation on titanium-based surfaces with rough topography.

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p8 attenuates the apoptosis induced by dihydroartemisinin in cancer cells through promoting autophagy

Cited by 37 publications

References 35 publications

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Artemisinin as an anticancer drug: Recent advances in target profiling and mechanisms of action

A Key Role of Autophagy in Osteoblast Differentiation on Titanium-Based Dental Implants

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