Curcumin Inhibits ROS Formation and Apoptosis in Methylglyoxal‐Treated Human Hepatoma G2 Cells

Chan, Wen‐Hsiung; Wu, Hsin-Jung; Hsuuw, Yan‐Der

doi:10.1196/annals.1338.057

Cited by 91 publications

(63 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[12][13][14][25][26][27][28] The anti-tumor role of MG may also be attributed to its effects on cell migration. 15 Our results showing that MG inhibited the viability, proliferation, migration, and invasion of DLD-1 and SW480 colon cancer cells while promoting their apoptosis are in accordance with previous results in other cancer types.…”

Section: Discussionmentioning

confidence: 99%

“…15 Our results showing that MG inhibited the viability, proliferation, migration, and invasion of DLD-1 and SW480 colon cancer cells while promoting their apoptosis are in accordance with previous results in other cancer types. [12][13][14][25][26][27][28] There are multiple potential mechanisms by which MG may induce tumor suppression: (1) inhibition of the synthesis of proteins and nucleic acids via irreversible modification of protein, DNA, and RNA;…”

Section: Discussionmentioning

confidence: 99%

“…11 MG induces apoptosis through multiple mechanisms such as accumulating reactive oxygen species and advanced glycation end products and triggering the mitochondrial apoptotic pathway. [12][13][14] MG also inhibits tumor metastasis, enhances the immune response, and increases sensitivity to anti-tumor agents. [15][16][17][18] c-Myc is one of the most widely expressed human protooncogenes and is frequently overexpressed in colon cancer.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Zhou

et al. 2016

Cancer Biology & Therapy

View full text Add to dashboard Cite

Methylglyoxal (MG) is a highly reactive dicarbonyl compound exhibiting anti-tumor activity. The antitumor effects of MG have been demonstrated in some types of cancer, but its role in colon cancer and the mechanisms underlying this activity remain largely unknown. We investigated its role in human colon cancer and the underlying mechanism using human colon cancer cells and animal model. Viability, proliferation, and apoptosis were quantified in DLD-1 and SW480 colon cancer cells by using the Cell Counting Kit-8, plate colony formation assay, and flow cytometry, respectively. Cell migration and invasion were assessed by wound healing and transwell assays. Glucose consumption, lactate production, and intracellular ATP production also were assayed. The levels of c-Myc protein and mRNA were quantitated by western blot and qRT-PCR. The anti-tumor role of MG in vivo was investigated in a DLD-1 xenograft tumor model in nude mice. We demonstrated that MG inhibited viability, proliferation, migration, and invasion and induced apoptosis of DLD-1 and SW480 colon cancer cells. Treatment with MG reduced glucose consumption, lactate production, and ATP production and decreased c-Myc protein levels in these cells. Moreover, MG significantly suppressed tumor growth and c-Myc expression in vivo. Our findings suggest that MG plays an anti-tumor role in colon cancer. It inhibits cancer cell growth by altering the glycolytic pathway associated with downregulation of c-Myc protein. MG has therapeutic potential in colon cancer by interrupting cancer metabolism.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Zhou

et al. 2016

Cancer Biology & Therapy

View full text Add to dashboard Cite

show abstract

“…The pro-oxidative effect of curcumin was observed in another study where curcumin at low concentrations reduced ROS formation in human myeloid leukemia cells and Hepatoma G2 cells, but elevated ROS levels at higher concentrations (7,8). In contrast, curcumin, as an anti-oxidant, inhibits ROS formation and apoptosis in human Hepatoma G2 cells and Chang liver cells ONCOLOGY REPORTS 23: 397-403, 2010 397 Curcumin induces apoptosis in human lung adenocarcinoma A549 cells through a reactive oxygen species-dependent mitochondrial signaling pathway (9,10). However, the precise signaling pathways for the ROS-mediated mitochondrial apoptotic cell death triggered by curcumin still remains unclear, especially in lung cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Curcumin induces apoptosis in human lung adenocarcinoma A549 cells through a reactive oxygen species-dependent mitochondrial signaling pathway

Chen

Wang²,

Xu³

et al. 2009

Oncol Rep

View full text Add to dashboard Cite

Abstract.Several studies have shown that curcumin can induce apoptosis and inhibit growth in human A549 lung adenocarcinoma cells. However, the mechanism is not completely understood yet. The present study was designed to investigate the effects of curcumin on A549 cells to better understand its apoptosis and apoptosis-related factors in vitro. The apoptosis induction, intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were examined by confocal fluorescence microscope and flow cytometry. The MAPK protein expression was examined by Western blot analysis. After treatment with curcumin, apoptosis were observed. Curcumin-induced apoptosis was accompanied by an increase of intracellular ROS level and a loss of MMP. In addition, induction of apoptosis was also accompanied by sustained phosphorylation and activation of JNK, p38 and ERK. However, pretreatment with MAPK inhibitors had no effect upon curcumin-induced apoptosis. GSH and NAC, an anti-oxidant agent, blocked the curcumin-induced ROS production, MMP loss and rescued cells from curcumininduced apoptosis. Our results indicated that curcumin induced apoptosis in A549 cells through a reactive oxygen speciesdependent mitochondrial signaling pathway and independent of MAPK signaling pathway.

show abstract

“…Curcumin, isolated from turmeric (Curcuma longa L.), contains curcumin as a major component but also contains demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC), respectively (4). Extensive research during the last half century has revealed several important functions of curcumin such as antioxidant, anti-inflammatory and anticancer properties (5)(6)(7). Recently, more and more studies have demonstrated the stronger activity of DMC when compared with curcumin in many aspects (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Demethoxycurcumin induces the apoptosis of human lung cancer NCI-H460 cells through the mitochondrial-dependent pathway

Lien

Liu

et al. 2015

Oncology Reports

View full text Add to dashboard Cite

Abstract. Lung cancer is the most common cause of cancerrelated mortality in the US as well as other regions of the world. Curcumin, demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC) are the major components of Curcuma longa L. It has been reported that curcumin inhibits the growth of various types of cancer cells in vitro and in vivo. However, the mechanisms involved in the inhibition of cell growth and induced apoptosis by DMC in human lung cancer cells remain unclear. In the present study, we investigated the effect of DMC on cell death via the induction of apoptosis in NCI-H460 human lung cancer cells. Flow cytometric assay was used to examine the total percentage of viable cells, the population of cells in the sub-G1 phase of the cell cycle, the level of reactive oxygen species (ROS), Ca 2+ production, mitochondrial membrane potential (ΔΨm) and caspase activity. Western blotting was used to examine the changes in the expression of cell cycle-and apoptosis-associated proteins. Confocal microscopy was used to examine the translocation of apoptosis-associated proteins. The results indicated that DMC significantly induced cell morphological changes and decreased the percentage of viable NCI-H460 cells and DMC induced apoptosis based on the cell distribution in the sub-G1 phase. Moreover, DMC promoted ROS and Ca 2+ production and decreased the level of ΔΨm and promoted the activities of caspase-3, -8 and -9. The Western blotting results showed that DMC promoted the expression of AIF, Endo G and PARP. The levels of Fas ligand (Fas L) and Fas were also upregulated. Furthermore, DMC promoted expression of ER stress-associated proteins such as GRP78, GADD153, IRE1β, ATF-6α, ATF-6β and caspase-4. Based on the findings, we suggest that DMC may be used as a novel anticancer agent for the treatment of lung cancer in the future.

show abstract

Curcumin Inhibits ROS Formation and Apoptosis in Methylglyoxal‐Treated Human Hepatoma G2 Cells

Cited by 91 publications

References 17 publications

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Methylglyoxal suppresses human colon cancer cell lines and tumor growth in a mouse model by impairing glycolytic metabolism of cancer cells associated with down-regulation of c-Myc expression

Curcumin induces apoptosis in human lung adenocarcinoma A549 cells through a reactive oxygen species-dependent mitochondrial signaling pathway

Demethoxycurcumin induces the apoptosis of human lung cancer NCI-H460 cells through the mitochondrial-dependent pathway

Contact Info

Product

Resources

About