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• W2920591119 endingPage "185" @default.
• W2920591119 startingPage "174" @default.
• W2920591119 abstract "Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma." @default.
• W2920591119 created "2019-03-11" @default.
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• W2920591119 date "2019-05-01" @default.
• W2920591119 modified "2023-10-15" @default.
• W2920591119 title "Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage" @default.
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• W2920591119 doi "https://doi.org/10.1016/j.ejphar.2019.03.004" @default.
• W2920591119 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30836068" @default.
• W2920591119 hasPublicationYear "2019" @default.
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