Antioral Cancer Effects by the Nitrated [6,6,6]Tricycles Compound (SK1) In Vitro

Chen, Yan‐Ning; Chan, Chieh‐Kai; Yen, Ching‐Yu; Shiau, Jun‐Ping; Chang, Meng‐Yang; Wang, Chung‐Cheng; Jeng, Jiiang‐Huei; Tang, Jen‐Yang; Chang, Hsueh-Wei

doi:10.3390/antiox11102072

Cited by 6 publications

(5 citation statements)

References 53 publications

(72 reference statements)

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“…This potential role of ROS was examined by the pretreatment of N -acetylcysteine (NAC), a ROS inhibitor [ 35 , 36 ]. Several anticancer studies, such as psoralidin [ 37 ], nitrated [ 6 , 6 , 6 ]tricycles compound SK1 [ 38 ], and Aaptos suberitoid extract [ 39 ], have demonstrated that NAC can reverse the ROS-induced apoptosis in the example of caspase 3/7 activation.…”

Section: Resultsmentioning

confidence: 99%

Synthesis and Anticancer Evaluation of 4-Anilinoquinolinylchalcone Derivatives

Yang

Lee

Chen

et al. 2023

IJMS

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A series of 4-anilinoquinolinylchalcone derivatives were synthesized and evaluated for antiproliferative activities against the growth of human cancer cell lines (Huh-7 and MDA-MB-231) and normal lung cells (MRC-5). The results exhibited low cytotoxicity against human lung cells (MRC-5). Among them, (E)-3-{4-{[4-(benzyloxy)phenyl]amino}quinolin-2-yl}-1-(4-methoxyphenyl) prop-2-en-1-one (4a) was found to have the highest cytotoxicity in breast cancer cells and low cytotoxicity in normal cells. Compound 4a causes ATP depletion and apoptosis of breast cancer MDA-MB-231 cells and triggers reactive oxygen species (ROS)-dependent caspase 3/7 activation. In conclusion, it is worth studying 4-anilinoquinolinylchalcone derivatives further as new potential anticancer agents for the treatment of human cancers.

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Section: Resultsmentioning

confidence: 99%

Synthesis and Anticancer Evaluation of 4-Anilinoquinolinylchalcone Derivatives

Yang

Lee

Chen

et al. 2023

IJMS

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“…Several anticancer reports demonstrated that antioxidant depletion was followed by ROS induction. For example, the nitrated [6,6,6]tricycle-derived compound SK1 triggered GSH depletion, leading to ROS overproduction in oral cancer cells [ 49 ]. Auranofin exhibits antiproliferation by ROS induction and GSH depletion in lung cancer cells [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Ginger-Derived 3HDT Exerts Antiproliferative Effects on Breast Cancer Cells by Apoptosis and DNA Damage

Chen

Shiau

et al. 2023

IJMS

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Ginger-derived compounds are abundant sources of anticancer natural products. However, the anticancer effects of (E)-3-hydroxy-1-(4′-hydroxy-3′,5′-dimethoxyphenyl)-tetradecan-6-en-5-one (3HDT) have not been examined. This study aims to assess the antiproliferation ability of 3HDT on triple-negative breast cancer (TNBC) cells. 3HDT showed dose-responsive antiproliferation for TNBC cells (HCC1937 and Hs578T). Moreover, 3HDT exerted higher antiproliferation and apoptosis on TNBC cells than on normal cells (H184B5F5/M10). By examining reactive oxygen species, mitochondrial membrane potential, and glutathione, we found that 3HDT provided higher inductions for oxidative stress in TNBC cells compared with normal cells. Antiproliferation, oxidative stress, antioxidant signaling, and apoptosis were recovered by N-acetylcysteine, indicating that 3HDT preferentially induced oxidative-stress-mediated antiproliferation in TNBC cells but not in normal cells. Moreover, by examining γH2A histone family member X (γH2AX) and 8-hydroxy-2-deoxyguanosine, we found that 3HDT provided higher inductions for DNA damage, which was also reverted by N-acetylcysteine. In conclusion, 3HDT is an effective anticancer drug with preferential antiproliferation, oxidative stress, apoptosis, and DNA damage effects on TNBC cells.

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“…It is helpful to combine other antioral cancer drugs with low cytotoxicity to normal cells, such as fucoidan, 28 manoalide, 69 and the nitrated [6,6,6]tricycles compound SK1. 70 Consequently, the combined treatment with two antioral cancer drugs with preferential antiproliferation may exert the synergistic antioral cancer effects.…”

Section: Discussionmentioning

confidence: 99%

The neddylation inhibitor MLN4924 inhibits proliferation and triggers apoptosis of oral cancer cells but not for normal cells

Chen,

Chan,

Shiau

et al. 2023

Environmental Toxicology

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Increased neddylation benefits the survival of several types of cancer cells. The inhibition of neddylation has the potential to exert anticancer effects but is rarely assessed in oral cancer cells. This study aimed to investigate the antiproliferation potential of a neddylation inhibitor MLN4924 (pevonedistat) for oral cancer cells. MLN4924 inhibited the cell viability of oral cancer cells more than that of normal oral cells (HGF‐1) with 100% viability, that is, IC50 values of oral cancer cells (CAL 27, OC‐2, and Ca9‐22) are 1.8, 1.4, and 1.9 μM. MLN4924 caused apoptotic changes such as the subG1 accumulation, activation of annexin V, pancaspase, and caspases 3/8/9 of oral cancer cells at a greater rate than in normal oral cells. MLN4924 induced greater oxidative stress in oral cancer cells compared to normal cells by upregulating reactive oxygen species and mitochondrial superoxide and depleting the mitochondrial membrane potential and glutathione. In oral cancer cells, preferential inductions also occurred for DNA damage (γH2AX and 8‐oxo‐2′‐deoxyguanosine). Therefore, this investigation demonstrates that MLN4924 is a potential anti‐oral‐cancer agent showing preferential inhibition of apoptosis and promotion of DNA damage with fewer cytotoxic effects on normal cells.

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Antioral Cancer Effects by the Nitrated [6,6,6]Tricycles Compound (SK1) In Vitro

Cited by 6 publications

References 53 publications

Synthesis and Anticancer Evaluation of 4-Anilinoquinolinylchalcone Derivatives

Synthesis and Anticancer Evaluation of 4-Anilinoquinolinylchalcone Derivatives

Ginger-Derived 3HDT Exerts Antiproliferative Effects on Breast Cancer Cells by Apoptosis and DNA Damage

The neddylation inhibitor MLN4924 inhibits proliferation and triggers apoptosis of oral cancer cells but not for normal cells

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