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JNK pathway mediates curcumin-induced apoptosis and autophagy in osteosarcoma MG63 cells.

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TLDR
The results suggest that autophagy may have an important role in resistance to apoptosis when MG63 cells are incubated with curcumin, and provide important insights into the interaction between apoptosis and Autophagy in osteosarcoma cells and clinical treatment strategies usingCurcumin.
Abstract
Human osteosarcoma is a common primary malignancy of the bone in children and adolescents It has been reported that curcumin is able to induce apoptosis in osteosarcoma MG63 cells through the mitochondrial pathway However, whether curcumin is able to induce autophagy and the interaction between apoptosis and autophagy in osteosarcoma cells has yet to be fully elucidated In the current study, it was determined that curcumin was able to significantly induce apoptosis, and lead to autophagy in MG63 cells Notably, inhibition of apoptosis enhanced curcumin-induced autophagy due to upregulation of the c-Jun N-terminal kinase (JNK) signaling pathway This finding was confirmed by the use of JNK-specific inhibitor, SP600125 Furthermore, our data showed that curcumin-induced apoptosis was increased when autophagy was completely inhibited by 3-methyladenine in MG63 cells These results suggest that autophagy may have an important role in resistance to apoptosis when MG63 cells are incubated with curcumin Thus, these results provide important insights into the interaction between apoptosis and autophagy in osteosarcoma cells and clinical treatment strategies using curcumin

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Curcumin: A naturally occurring autophagy modulator

TL;DR: This review will focus on how curcumin can target autophagy in different cellular settings that may extend the understanding of new pharmacological agents to overcome relevant diseases.
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Programmed Cell Death, from a Cancer Perspective: An Overview

TL;DR: A brief outline of PCD types as well as their role in cancer therapeutics is discussed, since irregularities in the cell death process are frequently found in various cancers, key proteins governing cell death type could be used as therapeutic targets for a wide range of cancer.
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Curcumin synergizes with 5-fluorouracil by impairing AMPK/ULK1-dependent autophagy, AKT activity and enhancing apoptosis in colon cancer cells with tumor growth inhibition in xenograft mice.

TL;DR: Pre-treatment with curcumin followed by 5-Fu may mediate autophagy turnover both in vitro and in vivo via AMPK/ULK1-dependent autophagic inhibition and AKT modulation, which may account for the increased susceptibility of the colon cancer cells/xenograft to the cytotoxicity of 5- Fu.
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Potential Mechanisms of Action of Curcumin for Cancer Prevention: Focus on Cellular Signaling Pathways and miRNAs.

TL;DR: An in-depth understanding of the anticancer mechanisms of curcumin will be helpful for developing this promising compound as a therapeutic agent in clinical management of cancer.
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Artesunate induces apoptosis and autophagy in HCT116 colon cancer cells, and autophagy inhibition enhances the artesunate‑induced apoptosis.

TL;DR: Findings suggested that the ART-induced autophagy may have a cytoprotective effect by suppressing apoptosis, and ART may be a potentially clinically useful anticancer drug for human colon cancer.
References
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Journal ArticleDOI

Signal transduction by the JNK group of MAP kinases.

TL;DR: This review will focus on the JNK group of MAP kinases, which are characterized by the sequence TEY and the two stress-activatedMAP kinases: p38 with the sequence TGY, and the c-Jun NH2-terminal kinases (JNK) with the sequences TPY.
Journal ArticleDOI

Bcl-2 antiapoptotic proteins inhibit Beclin 1-dependent autophagy.

TL;DR: Bcl-2 not only functions as an antiapoptotic protein, but also as an antiautophagy protein via its inhibitory interaction with Beclin 1, which may help maintain autophagy at levels that are compatible with cell survival, rather than cell death.
Journal ArticleDOI

The stress-activated protein kinase subfamily of c-Jun kinases.

TL;DR: The kinase p54s are the principal c-Jun N-terminal kinases activated by cellular stress and tumour necrosis factor (TNF)-α, hence they are designated stress-activated protein kinases, or SAPKs.
Journal ArticleDOI

Signal integration by JNK and p38 MAPK pathways in cancer development

TL;DR: This Review highlights the recent progress made in defining the functions of the JNK and p38 MAPK pathways in different cancers.
Journal ArticleDOI

Therapeutic Roles of Curcumin: Lessons Learned from Clinical Trials

TL;DR: Curcumin has shown protection against hepatic conditions, chronic arsenic exposure, and alcohol intoxication, and dose-escalating studies have indicated the safety of curcumin at doses as high as 12 g/day over 3 months.
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