Tomentosin Displays Anti-Carcinogenic Effect in Human Osteosarcoma MG-63 Cells via the Induction of Intracellular Reactive Oxygen Species

Lee, Chang Min; Lee, Jongsung; Nam, Myeong Jin; Choi, Youn Soo; Park, See‐Hyoung

doi:10.3390/ijms20061508

Cited by 27 publications

(31 citation statements)

References 47 publications

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“…Thus, under oxidative stress conditions, biomolecules may undergo the attack of ROS and get oxidized. Most of the time, such phenomena are deleterious for cells, but in some case, inducing an overproduction of ROS can help kill cells such as cancer cells [24].…”

Section: Production Of Rosmentioning

confidence: 99%

Chemical Basis of Reactive Oxygen Species Reactivity and Involvement in Neurodegenerative Diseases

Collin

2019

IJMS

582

357

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Increasing numbers of individuals suffer from neurodegenerative diseases, which are characterized by progressive loss of neurons. Oxidative stress, in particular, the overproduction of Reactive Oxygen Species (ROS), play an important role in the development of these diseases, as evidenced by the detection of products of lipid, protein and DNA oxidation in vivo. Even if they participate in cell signaling and metabolism regulation, ROS are also formidable weapons against most of the biological materials because of their intrinsic nature. By nature too, neurons are particularly sensitive to oxidation because of their high polyunsaturated fatty acid content, weak antioxidant defense and high oxygen consumption. Thus, the overproduction of ROS in neurons appears as particularly deleterious and the mechanisms involved in oxidative degradation of biomolecules are numerous and complexes. This review highlights the production and regulation of ROS, their chemical properties, both from kinetic and thermodynamic points of view, the links between them, and their implication in neurodegenerative diseases.

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Section: Production Of Rosmentioning

confidence: 99%

Chemical Basis of Reactive Oxygen Species Reactivity and Involvement in Neurodegenerative Diseases

Collin

2019

IJMS

582

357

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“…After 24 h of incubation, the cells were treated with acetylshikonin at a concentration gradient of 0 to 10 μM and incubated for 24, 48, and 72 h for the time-dependent response assay. After 24, 48, and 72 h of treatment, a 20 μL MTT dye solution (5 mg/mL in phosphate buffer) was added to each well and the incubation for 2 h. After all the media were removed, formazan was solubilized in 200 μL DMSO, and light absorbance was measured at a wavelength of 570 nm using a microplate reader [31].…”

Section: Mtt Cell Viability Assaymentioning

confidence: 99%

Acetylshikonin Induces Apoptosis in Human Colorectal Cancer HCT‐15 and LoVo Cells via Nuclear Translocation of FOXO3 and ROS Level Elevation

Lim

Lee

Nam

et al. 2021

Oxidative Medicine and Cellular Longevity

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Acetylshikonin, a naphthoquinone, is a pigment compound derived from Arnebia sp., which is known for its anti-inflammatory potential. However, its anticarcinogenic effect has not been well investigated. Thus, in this study, we focused on investigating its apoptotic effects against HCT-15 and LoVo cells, which are human colorectal cancer cells. MTT assay, cell counting assay, and colony formation assay have shown acetylshikonin treatment induced cytotoxic and antiproliferative effects against colorectal cancer cells in a dose- and time-dependent manner. DNA fragmentation was observed via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Also, the increase of subG1 phase in cell cycle arrest assay and early/late apoptotic rates in annexin V/propidium iodide (PI) double staining assay was observed, which indicates an apoptotic potential of acetylshikonin against colorectal cancer cells. 2 ′ ,7 ′ -Dichlorofluorescin diacetate (DCF-DA) staining was used to evaluate reactive oxygen species (ROS) generation in acetylshikonin-treated colorectal cancer cells. Fluorescence-activated cell sorting (FACS) analysis showed that acetylshikonin induced an increase in reactive oxygen species (ROS) levels and apoptotic rate in a dose- and time-dependent manner in HCT-15 and LoVo cells. In contrast, cotreatment with N-acetyl cysteine (NAC) has reduced ROS generation and antiproliferative effects in colorectal cancer cells. Western blotting analysis showed that acetylshikonin treatment induced increase of cleaved PARP, γH2AX, FOXO3, Bax, Bim, Bad, p21, p27, and active forms of caspase-3, caspase-7, caspase-9, caspase-6, and caspase-8 protein levels, while those of inactive forms were decreased. Also, the expressions of pAkt, Bcl-2, Bcl-xL, peroxiredoxin, and thioredoxin 1 were decreased. Furthermore, western blotting analysis of cytoplasmic and nuclear fractionated proteins showed that acetylshikonin treatment induced the nuclear translocation of FOXO3, which might result from DNA damage by the increased intracellular ROS level. This study represents apoptotic potential of acetylshikonin against colorectal cancer cells via translocation of FOXO3 to the nucleus and upregulation of ROS generation.

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“…13 Furthermore, our laboratory reported that tomentosin induces apoptosis in osteosarcoma cancer cells by generating reactive oxygen species. 30 However, the anticarcinogenic effects of tomentosin in HCC have not been studied well.…”

Section: Discussionmentioning

confidence: 99%

Induction of cell cycle arrest and apoptosis by tomentosin in hepatocellular carcinoma HepG2 and Huh7 cells

Lee

et al. 2020

Hum Exp Toxicol

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Tomentosin, a sesquiterpene lactone, is known to possess various biological activities. However, its anticarcinogenic activity against human hepatocellular carcinoma (HCC) cells has not been investigated in detail. Thus, this study aimed to elucidate the cytotoxic mechanism of tomentosin in human HCC cell lines HepG2 and Huh7. WST-1, cell counting, and colony formation assay results showed that treatment with tomentosin decreased the viability and suppressed the proliferation rate of HepG2 and Huh7 cells in a dose- and time-dependent manner. Cell cycle analysis revealed increased population of cells at the SubG1 and G2/M stage, and decreased population of cells at the G0/1 stage in HepG2 and Huh7 cells treated with tomentosin. Annexin V/propidium iodide double staining and TUNEL assay results showed increased apoptotic cell population and DNA fragmentation in HepG2 and Huh7 cells treated with tomentosin. Western blotting analysis results showed that tomentosin treatment significantly increased the expression level of Bax, Bim (short form), cleaved PARP1, FOXO3, p53, pSer15p53, pSer20p53, pSer46p53, p21, and p27, but decreased the expression of Bcl2, caspase3, caspase7, caspase9, cyclin-dependent kinase 2 (CDK2), CDK4, CDK6, cyclinB1, cyclinD1, cyclinD2, cyclinD3, and cyclinE in a dose-dependent manner. Taken together, this study revealed that tomentosin, which acted through cell cycle arrest and apoptosis, may be a useful therapeutic option against HCC.

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Tomentosin Displays Anti-Carcinogenic Effect in Human Osteosarcoma MG-63 Cells via the Induction of Intracellular Reactive Oxygen Species

Cited by 27 publications

References 47 publications

Chemical Basis of Reactive Oxygen Species Reactivity and Involvement in Neurodegenerative Diseases

Chemical Basis of Reactive Oxygen Species Reactivity and Involvement in Neurodegenerative Diseases

Acetylshikonin Induces Apoptosis in Human Colorectal Cancer HCT‐15 and LoVo Cells via Nuclear Translocation of FOXO3 and ROS Level Elevation

Induction of cell cycle arrest and apoptosis by tomentosin in hepatocellular carcinoma HepG2 and Huh7 cells

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