Curcumin induces apoptosis in human neuroblastoma cells via inhibition of AKT and Foxo3a nuclear translocation

Picone, Pasquale; Nuzzo, Domenico; Caruana, Luca; Messina, Elisa; Scafidi, V.; Carlo, Marta Di

doi:10.3109/10715762.2014.960410

Cited by 34 publications

(31 citation statements)

References 48 publications

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“…Curcumin treatment also reduced HSP60 and hexokinase II mitochondrial protein levels and increased the proapoptotic protein, Bcl‐2 associated death promoter (BAD). Curcumin's antitumor effect is modulated via phosphatase and tensin homolog (PTEN) and inhibition of the Akt cell signaling pathway, thereby activating the expression of proapototic genes (p27, Bim, and Fas‐L) …”

Section: Hsp60 and Cancermentioning

confidence: 99%

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Modulatory effects of curcumin on heat shock proteins in cancer: A promising therapeutic approach

et al. 2019

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Cancer metastasis represents a multistep process, including alteration of cell adhesion/motility in the microenvironment and sustained angiogenesis, which is essential for supporting cancer growth in tissues that are distant from the primary tumor. There is growing evidence suggesting that heat shock proteins (HSPs) (also known as heat stress proteins), which constitute a family of stress‐inducible proteins, may be involved in the pathogenesis of cancer. Curcumin (diferuloylmethane) is a potent anti‐inflammatory, antioxidant, antimicrobial, and antitumor agent. Curcumin has been shown to regulate different members of HSPs including HSP27, HSP40, HSP60, HSP70, and HSP90 in cancer. Here, we present extent findings suggesting that curcumin may act as a potential therapeutic agent for the treatment of cancer through its regulation of HSPs.

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Section: Hsp60 and Cancermentioning

confidence: 99%

“…Curcumin's antitumor effect is modulated via phosphatase and tensin homolog (PTEN) and inhibition of the Akt cell signaling pathway, thereby activating the expression of proapototic genes (p27, Bim, and Fas-L). 113…”

Section: -(4-pyridinylmethylene) Curcumin (C1206)mentioning

confidence: 99%

Modulatory effects of curcumin on heat shock proteins in cancer: A promising therapeutic approach

et al. 2019

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“…Curcumin treatment caused a rapid increase in reactive oxygen species (ROSs) and a decrease in mitochondrial membrane potential, events leading to apoptosis activation. Furthermore, curcumin induced a decrease in heat shock protein (HSP) 60 and hexokinase II mitochondrial protein levels and an increase in the proapoptotic protein, bcl-2-associated death promoter [4 in a dose and time-dependent manner. Curcumininduced apoptosis was ascribed to JNKs, as hindering their activity abolished poly(ADP-ribose) polymerase (PARP) fragmentation [5].…”

Section: Preclinical Studiesmentioning

confidence: 99%

An update on Curcuma as a functional food in the control of cancer and inflammation

Schaffer

Bar-Sela

2015

Current Opinion in Clinical Nutrition and Metabolic Care

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“…Nuclear translocation of PKM2 is instrumental in promoting cell proliferation and development, and p-Akt translocation into the nucleus plays an important role in inhibiting cellular apoptosis [11,35]. Detection of renal nuclear proteins in Figure 5A shows that heat stress induced the most PKM2 translocation into the nucleus, followed by GA, TR, GA+HS, and TR+HS.…”

Section: The Nuclear Pkm2 Akt P-akt and Hsf-1 Is Also Altered For mentioning

confidence: 99%

“…Stressful stimuli generates potentially harmful ROS above a physiological threshold, and apoptosis is often a consequence of reactive oxygen species (ROS) generation, triggering cell loss and inducing tissue injury [11]. Several types of stimuli can cause apoptosis and autophagy in the same cell.…”

Section: Introductionmentioning

confidence: 99%

Hsp90 Relieves Heat Stress-Induced Damage in Mouse Kidneys: Involvement of Antiapoptotic PKM2-AKT and Autophagic HIF-1α Signaling

Chen

Yang

Zhu

et al. 2020

IJMS

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Heat stress can particularly affect the kidney because of its high rate of adenosine triphosphate consumption. Competition between apoptosis and autophagy-mediated survival always exists in damaged tissue. And Hsp90 can enhance cellular protection to resist heat stress. However, the relationship between Hsp90 and the above competition and its underlying mechanism in the kidney are unclear. The present study found that heat stress induced obvious histopathological and oxidative injury, which was connected with cellular apoptosis and autophagy in the kidney and was associated with the levels of Hsp90 expression or function. The data showed that during heat stress, Hsp90 activated the PKM2-Akt signaling pathway to exert antiapoptotic effects and induce Hsp70 expression regulated by HSF-1, stimulated autophagy-mediated survival through the HIF-1α-BNIP3/BNIP3L pathway, and finally protected the kidney from heat-stress injury. Moreover, the nuclear translocation of PKM2, (p-) Akt, HSF-1, and HIF-1α was enhanced by heat stress, but only intranuclear p-Akt and HSF-1 were specifically influenced by Hsp90, contributing to regulate the cellular ability of resisting heat-stress damage. Our study provided new insights regarding the molecular mechanism of Hsp90 in the kidney in response to heat-stress injury, possibly contributing to finding new targets for the pharmacological regulation of human or animal acute kidney injury from heat stress in future research.Autophagy, a lysosomal degradation pathway, is an essential cellular adaptation mechanism for avoiding oxidative damage. Studies of the role of autophagy in AKI have reported both beneficial and detrimental effects [12][13][14]. Light chain 3 (LC3), is essential for autophagy and serves as a vital component in monitoring autophagy and visualizing autophagosomes in vivo [15]. Pyruvate kinase M2 isoform (PKM2), a rate-limiting terminal glycolytic enzyme, catalyzes the last step of glycolysis, and recent studies have reported that PKM2 is associated with the Akt signal pathway, which regulates cell survival and apoptosis [16,17]. Meanwhile, many cellular signals have been reported to be involved in the regulation of autophagy, including the Akt (protein kinase B)-mTOR (mammalian target of rapamycin) pathway [18,19]. Furthermore, Akt also plays a vital role in resisting heat stress-induced apoptosis [20]. Hypoxia-inducible factor (HIF), especially HIF-1α, is also a major actor in the cell survival autophagy in response to hypoxia stress via BNIP3 (Bcl-2/adenovirus E1B 19-kDa interacting protein 3) and BNIP3L (Bcl-2/adenovirus E1B 19-kDa interacting protein 3 like) [21]. However, understanding the roles and their interplay of autophagy and apoptosis, and identification of the closely related signaling pathways in the kidney, is still very deficient but important for controlling tissue damage during heat stress.At the cellular level, tolerance to heat stress is mainly regulated by heat shock proteins (HSPs), which are also synthesized under various environmental and oxidative...

show abstract

Curcumin induces apoptosis in human neuroblastoma cells via inhibition of AKT and Foxo3a nuclear translocation

Cited by 34 publications

References 48 publications

Modulatory effects of curcumin on heat shock proteins in cancer: A promising therapeutic approach

Modulatory effects of curcumin on heat shock proteins in cancer: A promising therapeutic approach

An update on Curcuma as a functional food in the control of cancer and inflammation

Hsp90 Relieves Heat Stress-Induced Damage in Mouse Kidneys: Involvement of Antiapoptotic PKM2-AKT and Autophagic HIF-1α Signaling

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