Gingerenone A Induces Antiproliferation and Senescence of Breast Cancer Cells

Yu, Tsan-Jung; Tang, Jen‐Yang; Shiau, Jun‐Ping; Hou, Ming‐Feng; Yen, Chia-Hung; Ou‐Yang, Fu; Chen, Chung‐Yi; Chang, Hsueh-Wei

doi:10.3390/antiox11030587

Cited by 20 publications

(17 citation statements)

References 54 publications

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“…6-shogaol showed an IC 50 value of 23.3 μM in breast cancer cells (MCF7) in a 72 h sulforhodamine B assay [ 37 ]. Gingerenone A showed IC 50 values of 61.4 and 76.1 μM in breast cancer cells MCF7 and MDA-MB-231, respectively, in a 48 h MTS assay [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

“…In addition to antiproliferation and antioxidant regulation, oxidative stress is commonly associated with apoptosis [ 46 , 51 ] and DNA damage [ 18 , 52 , 53 , 54 ]. For example, sinularin triggers preferential oxidative stress, leading to the preferential apoptosis and DNA damage of breast cancer cells but not normal cells [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, several ginger-derived compounds exhibit an oxidative-stress-generating ability for killing cancer cells. For example, gingerenone A inhibits the proliferation of breast cancer cells by upregulating oxidative stress [ 18 ], and 6-gingerol triggers oxidative stress and inhibits the proliferation of gastric cancer cells [ 19 ]. However, several ginger-derived compounds have not been fully investigated regarding their medicinal effects.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…Then, the luminescent signaling from the ATP reaction was assessed by a CentroLIApc LB 962 Luminometer (Berthold Technologies GmbH & Co, Bad Wildbad, KG., Germany). Additionally, cell numbers were determined by trypan blue exclusion assay (final concentration 0.2%) [ 39 ]. The synergy between UVC and PHA was calculated as previously described [ 40 ], i.e., the synergy (α) = survival fraction for UVC × survival fraction for PHA/(survival fraction for UVC/PHA).…”

Section: Methodsmentioning

confidence: 99%

Combined Treatment (Ultraviolet-C/Physapruin A) Enhances Antiproliferation and Oxidative-Stress-Associated Mechanism in Oral Cancer Cells

et al. 2022

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Physapruin A (PHA), a Physalis peruviana-derived withanolide, exhibits antiproliferation activity against oral and breast cancer cells. However, its potential antitumor effects in combined treatments remain unclear. This investigation focused on evaluating the impact of the combined treatment of ultraviolet-C with PHA (UVC/PHA) on the proliferation of oral cancer cells. The UVC-caused antiproliferation was enhanced by combination with PHA in oral cancer (Ca9-22 and CAL 27) but not normal cells (SG), as evidenced by ATP detection, compared with UVC or PHA alone. UVC/PHA showed a greater extent of subG1 increase, G2/M arrest, annexin-V-assessed apoptosis, caspase 3/7 activation, and reactive oxygen species (ROS) in the UVC or PHA treatment of oral cancer compared to normal cells. Moreover, the mitochondrial functions, such as mitochondrial superoxide bursts and mitochondrial membrane potential destruction, of oral cancer cells were also enhanced by UVC/PHA compared to UVC or PHA alone. These oxidative stresses triggered γH2AX and 8-hydroxyl-2’-deoxyguanosine-assessed DNA damage to a greater extent under UVC/PHA treatment than under UVC or PHA treatment alone. The ROS inhibitor N-acetylcysteine reversed all these UVC/PHA-promoted changes. In conclusion, UVC/PHA is a promising strategy for decreasing the proliferation of oral cancer cells but shows no inhibitory effect on normal cells.

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“…Apigenin inhibits oxidative stress-triggered senescence of lung fibroblasts [ 357 ]. Gingerenone A, a ginger-derived compound, inhibits proliferation and triggers oxidative stress and senescence of breast cancer cells, reverted by N -acetylcysteine [ 358 ].…”

Section: Natural Products Regulate Oxidative Stress-modulated Cell Fu...mentioning

confidence: 99%

The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products

et al. 2022

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Oxidative stress and AKT serine-threonine kinase (AKT) are responsible for regulating several cell functions of cancer cells. Several natural products modulate both oxidative stress and AKT for anticancer effects. However, the impact of natural product-modulating oxidative stress and AKT on cell functions lacks systemic understanding. Notably, the contribution of regulating cell functions by AKT downstream effectors is not yet well integrated. This review explores the role of oxidative stress and AKT pathway (AKT/AKT effectors) on ten cell functions, including apoptosis, autophagy, endoplasmic reticulum stress, mitochondrial morphogenesis, ferroptosis, necroptosis, DNA damage response, senescence, migration, and cell-cycle progression. The impact of oxidative stress and AKT are connected to these cell functions through cell function mediators. Moreover, the AKT effectors related to cell functions are integrated. Based on this rationale, natural products with the modulating abilities for oxidative stress and AKT pathway exhibit the potential to regulate these cell functions, but some were rarely reported, particularly for AKT effectors. This review sheds light on understanding the roles of oxidative stress and AKT pathway in regulating cell functions, providing future directions for natural products in cancer treatment.

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Gingerenone A Induces Antiproliferation and Senescence of Breast Cancer Cells

Cited by 20 publications

References 54 publications

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

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

Combined Treatment (Ultraviolet-C/Physapruin A) Enhances Antiproliferation and Oxidative-Stress-Associated Mechanism in Oral Cancer Cells

The Impact of Oxidative Stress and AKT Pathway on Cancer Cell Functions and Its Application to Natural Products

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