Emodin Suppresses the Migration and Invasion of Melanoma Cells

Liu, Chi; Chen, Liang; Wang, Wan-Chen; Qin, Dengke; Jia, Chuanlong; Yuan, Mingjie; Wang, Heng; Guo, Yu; Zhu, Jingjing; Zhou, Yiqun; Zhao, Hongbin; Liu, Tianyi

doi:10.1248/bpb.b20-00807

Cited by 10 publications

(7 citation statements)

References 47 publications

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“…The anticarcinogenic activities of chrysophanol were also elaborated in diverse tumors, including colorectal can- cer [21] and oral cancer [22]. Moreover, Liu et al [23] reported that emodin inhibits cell proliferation, migration, and invasion with promoted apoptotic of B16F10 and A375 melanoma cells. Similar anti-cancer role of emodin and physcion was also observed in A375 melanoma cells [24].…”

Section: Discussionmentioning

confidence: 99%

Chrysophanol induces cell apoptosis and suppresses cell invasion by regulating AKT and MAPK signaling pathway in melanoma cells

Guan¹,

Huang²

2022

ScienceAsia

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Melanoma is a highly heterogeneous and invasive tumor with poor prognosis due to its resistance to radiotherapy, chemotherapy, and immunotherapy. Chrysophanol has the anti-carcinogenic role in a variety of tumors. Although the anti-proliferative role of chrysophanol in melanoma has been reported, its specific molecular mechanisms are still unclear. In the present study, the proliferation, migration, invasion, apoptosis, and cell cycle of A375 and A2058 cells were evaluated through MTT, colony formation, cell scratch, Transwell, and flow cytometry assays. Besides, the relative levels of proteins related to AKT and MAPK signaling pathway were determined by western blotting. The results revealed that chrysophanol significantly inhibited cell viability, colony formation, and cell invasive but increased the relative wound width of A375 and A2058 cells. Chrysophanol also notably enhanced the apoptotic rate, accompanied with the induced protein levels of Bax and Cleaved caspase-3 and reduced protein level of Bcl-2. In addition, chrysophanol observably promoted the ratio of G0/G1 phase, while restrained the relative protein expressions of Cyclin D1 and CDK4. Furthermore, the relative expressions of p-AKT/AKT, p-ERK1/2/ERK1/2, and p-JNK/JNK were significantly decreased, and the relative expression of p-38/38 was enhanced by 20, 50, and 100 µM chrysophanol treatment. Totally, the dose-dependent effects of chrysophanol on melanoma cell proliferation, migration, invasion, apoptosis, and cell cycle were observed. To sum up, these results revealed that chrysophanol induced cell apoptosis and suppressed cell invasion by regulating AKT and MAPK signaling pathway in both A375 and A2058 cells in a dosedependent manner.

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Section: Discussionmentioning

confidence: 99%

Chrysophanol induces cell apoptosis and suppresses cell invasion by regulating AKT and MAPK signaling pathway in melanoma cells

Guan¹,

Huang²

2022

ScienceAsia

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“…It is known that β-catenin and MMPs are involved in multiple regulatory processes related to cell migration and invasion [ 46 , 47 , 48 ]. Cell metastasis involves complex processes, including degradation of the extracellular cell matrix (ECM), separation of cells, adhesion of cells to endothelial cells, cell migration, cell invasion, cell motility and rebuilding of the growing system at a distance site [ 58 ]. Through the above processes, the degradation of the ECM is the key step in cell migration and invasion, a biochemical and biophysical barrier to cell migration and invasion and a major phenotype of cancer metastasis [ 59 ].…”

Section: Discussionmentioning

confidence: 99%

Suppressive Effects of Siegesbeckia orientalis Ethanolic Extract on Proliferation and Migration of Hepatocellular Carcinoma Cells through Promoting Oxidative Stress, Apoptosis and Inflammatory Responses

et al. 2022

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Previous studies have demonstrated that Siegesbeckia orientalis (SO) has a suppressive effect on the growth and migration of endometrial and cervical cancer cells. The present study examined the effect of SO ethanolic extract (SOE) on the proliferation and migration of hepatocellular carcinoma (HCC) and examined the effects of SOE on non-cancerous cells using HaCaT keratinocytes as a model. The SOE effectively inhibited the proliferation of Hepa1-6 (IC50 = 282.4 μg/mL) and HepG2 (IC50 = 344.3 μg/mL) hepatoma cells, whereas it has less cytotoxic effect on HaCaT cells (IC50 = 892.4 μg/mL). The SOE treatment increased the generation of ROS in HCC, but decreased the expression of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and catalase. In contrast, it reduced intracellular ROS formation and upregulated the expression of the related antioxidant enzymes in the H2O2-stimulated HaCaT cells. The SOE intervention also down-regulated the anti-apoptotic Bcl-2 and the migration-related proteins including matrix metalloproteinases (MMPs) and b-catenin in the HCC, suggesting that SOE could promote HCC apoptosis and inhibit HCC migration. On the contrary, it reduced apoptosis and promoted the migration of the keratinocytes. Additionally, the SOE treatment significantly up-regulated the pro-inflammatory cytokines, including TNF-a, IL-6 and IL-1b, in Hepa1-6 and HepG2 cells. Conversely, it significantly decreased the expression of these cytokines in the H2O2-induced HaCaT cells. These findings indicated that SOE treatment can delay the progression of HCC by increasing oxidative stress, promoting inflammatory response, inducing cancer cell apoptosis and inhibiting their migration. It also has protective effects from pro-oxidant H2O2 in non-cancerous cells. Therefore, SOE may provide a potential treatment for liver cancer.

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“…Li et al . found that emodin had significant antiproliferation and proapoptotic activities on B16F10 and A375 melanoma cells with strong metastatic ability and significantly inhibited the migration and invasion of tumor cells 251 .…”

Section: Anticancer Effects Of Emodinmentioning

confidence: 93%

The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers

et al. 2022

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Cancers are generally recognized as the leading cause of death and a predominant barrier to prolonging life expectancy in both developed and developing countries. Emodin is a typical anthraquinone derivative from various plants that exhibits a wide spectrum of biological activities, such as anticancer, antibacterial, hepatoprotective and anti-inflammatory activities. Much previous preclinical evidence has demonstrated that emodin exhibits reliable effects on several cancer types, including lung cancer, liver cancer, colon cancer, breast cancer, pancreatic cancer, leukemia, cervical cancer, and ovarian cancer, etc . The related molecular mechanisms corresponding to the anticancer activities of emodin are involved in the induction of apoptosis, inhibition of cell proliferation, enhanced reactive oxygen species (ROS) accumulation, and induction of autophagy, etc . In the present review, we summarized the sources, anticancer properties in vitro and in vivo , molecular mechanisms, metabolic transformation and toxicities of emodin. In addition, we also discussed the limitations of the present investigations of emodin against cancers and gave some perspectives for them, which would be beneficial for the further exploration and development of this natural compound as a clinical cancer drug.

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Emodin Suppresses the Migration and Invasion of Melanoma Cells

Cited by 10 publications

References 47 publications

Chrysophanol induces cell apoptosis and suppresses cell invasion by regulating AKT and MAPK signaling pathway in melanoma cells

Chrysophanol induces cell apoptosis and suppresses cell invasion by regulating AKT and MAPK signaling pathway in melanoma cells

Suppressive Effects of Siegesbeckia orientalis Ethanolic Extract on Proliferation and Migration of Hepatocellular Carcinoma Cells through Promoting Oxidative Stress, Apoptosis and Inflammatory Responses

The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers

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