Reversine inhibits <scp>MMP</scp>‐1 and <scp>MMP</scp>‐3 expressions by suppressing of <scp>ROS</scp>/<scp>MAPK</scp>/<scp>AP</scp>‐1 activation in <scp>UV</scp>‐stimulated human keratinocytes and dermal fibroblasts

Kim, Jeong-Mi; Kim, Sun Young; Noh, Eun‐Mi; Song, Hak Jun; Lee, Guemsan; Kwon, Kang‐Beom; Lee, Young‐Rae

doi:10.1111/exd.13494

Cited by 37 publications

(28 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…11,27,28 Kim et al report that UVB stimulates the generation of reactive oxygen species (ROS). 29 This study found that the levels of ROS and MMP depolarization in the VitK3-UVB group was significantly higher than individual treatment groups. That is to say, VitK3-UVB induces apoptosis in A431 cells by increasing ROS and altering MMP.…”

Section: Discussionmentioning

confidence: 65%

<p>Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells</p>

Shi¹,

Zheng²,

Yang³

et al. 2020

OTT

View full text Add to dashboard Cite

Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer and its incidence continues to rise yearly. Photodynamic therapy (PDT) is a noninvasive form of cancer therapy, which utilizes the combined action of a photosensitizer, light, and oxygen molecules to selectively cause cellular damage to tumor cells. Vitamin K3 (VitK3) has been shown to induce apoptosis and inhibit the growth of tumor cells in humans. The purpose of this study was to determine the effect of VitK3 and ultraviolet radiation B (UVB) on oxidative damage, proliferation and apoptosis of A431 cells. Methods: CCK-8 assay was used to detect cell proliferation; Hoechst staining, TUNEL assay and flow cytometry analysis were used to detect apoptosis. Western Blot was perfomed to measure the expression of apoptosis-related proteins. Flow cytometry analysis was employed to detect the reactive oxygen species (ROS) levels and mitochondrial membrane potential. Finally, the role of VitK3 in combination with UVB on the proliferation and apoptosis of A431 cells was investigated using mice xenograft models. Results: We found that the co-treatment of VitK3 combined with UVB more significantly inhibited the growth and proliferation of A431 cells than either VitK3 or UVB alone. Hoechst 33258 staining and flow cytometry analysis revealed that apoptosis was more pronounced in the VitK3-UVB group compared to the VitK3 and UVB groups. Moreover, flow cytometry analysis showed that ROS and the depolarization of the mitochondrial membrane potential were higher in all the co-treatment groups compared to the control, VitK3, and UVB groups. The VitK3-UVB group exhibited a significantly lower tumor growth rate in mouse xenograft models. Conclusion: This study reveals that VitK3 combined with UVB inhibits the growth and induces apoptosis of A431 cells in vitro and suppresses tumor growth and promotes apoptosis of cSCC in vivo.

show abstract

Section: Discussionmentioning

confidence: 65%

<p>Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells</p>

Shi¹,

Zheng²,

Yang³

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…erefore, researches focused on developing MMP inhibitors as antiphotoaging agents to prevent the UVB-induced degradation of the skin collagen [24,25]. Several studies reported very promising results indicating Evidence-Based Complementary and Alternative Medicine that ameliorating the MMP overexpression is a beneficial strategy against photoaging along with scavenging the UVBinduced ROS [26,27]. Keratinocytes form the main defense mechanism of skin against UVB irradiation as UVB rays mainly affect epidermis layer.…”

Section: Discussionmentioning

confidence: 99%

Antiphotoaging Effects of 3,5-Dicaffeoyl-epi-quinic Acid via Inhibition of Matrix Metalloproteinases in UVB-Irradiated Human Keratinocytes

Lee

Karadeniz

et al. 2020

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

UVB exposure is one of the causes of several skin complications including but not limited to premature aging, wrinkle formation, and hyperpigmentation. UV-induced skin aging is called photoaging, and oxidative stress-induced overexpression of matrix metalloproteinases (MMPs) is the main reason behind the photoaging-mediated collagen degradation. Natural origin inhibitors of MMPs are regarded as a promising approach to prevent or treat photoaging. Therefore, the present study investigated the protective effects of 3,5-dicaffeoyl-epi-quinic acid (DCEQA) in human HaCaT keratinocytes against UVB irradiation-related dysregulation of MMPs. Changes in the mRNA and protein expression and release of MMP-1, -2, and -9 were observed after UVB irradiation with or without DCEQA treatment. In addition, the effect of DCEQA on the activation of p38, JNK, and ERK MAPKs was analyzed. Treatment of UVB-irradiated HaCaT cells with 10 μM DCEQA significantly suppressed the overexpression of both mRNA and protein of MMP-1, -2, and -9 while slightly increasing the diminished type I procollagen production. UVB-induced activation of MAPKs was also ameliorated by DCEQA treatment in a dose-dependent manner. Results indicated that DCEQA treatment was able to protect keratinocytes from UVB-induced photoaging by inhibiting the stimulated production of MMPs and the related decrease in collagen production. It was suggested that DCEQA downregulated the collagen degradation via inhibition of MAPK activation, which resulted in decreased MMP activity.

show abstract

“…UVB irradiation induces oxidative damage by triggering the MAPK signaling pathway through the phosphorylation of the JNK, ERK, and p38 signaling cascades [ 37 ]. The activation of the MAPKs activates the transcription of AP-1 and NF-κB [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Euphrasia officinalis Extract against Ultraviolet B-Induced Photoaging in Normal Human Dermal Fibroblasts

Liu

Hwang

Ngo

et al. 2018

IJMS

View full text Add to dashboard Cite

Ultraviolet (UV) radiation induces skin photoaging, which is associated with the elevation of matrix metalloproteinases (MMPs) and the impairment of collagen. The Euphrasia species play a well-known role in the treatment of certain eye disorders through their anti-oxidative and anti-inflammatory activities. However, their protective activity toward UVB-induced damage remains unclear. In the present study, we investigated the protective effect of Euphrasia officinalis (95% ethanol extract) on UVB-irradiated photoaging in normal human dermal fibroblasts (NHDFs). Our results show that Euphrasia officinalis extract exhibited obvious reactive oxygen species (ROS) and 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical scavenging activity, enhanced NHDF cell migration, and reduced UVB-induced apoptosis. The UVB-induced increases in MMP-1 and MMP-3 and decrease in type I procollagen were ameliorated by Euphrasia officinalis treatment, which worked by suppressing the mitogen-activated protein kinase (MAPK) and nuclear transcription factor activator protein 1 (AP-1) signaling pathways. Taken together, our data strongly suggest that Euphrasia officinalis ethanol extract could reduce UVB-induced photoaging by alleviating oxidative stress, proinflammatory activity, and cell apoptosis.

show abstract

Reversine inhibits MMP‐1 and MMP‐3 expressions by suppressing of ROS/MAPK/AP‐1 activation in UV‐stimulated human keratinocytes and dermal fibroblasts

Cited by 37 publications

References 32 publications

<p>Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells</p>

<p>Effects of Vitamin K3 Combined with UVB on the Proliferation and Apoptosis of Cutaneous Squamous Cell Carcinoma A431 Cells</p>

Antiphotoaging Effects of 3,5-Dicaffeoyl-epi-quinic Acid via Inhibition of Matrix Metalloproteinases in UVB-Irradiated Human Keratinocytes

Protective Effects of Euphrasia officinalis Extract against Ultraviolet B-Induced Photoaging in Normal Human Dermal Fibroblasts

Contact Info

Product

Resources

About