The inhibitory mechanism by curcumin on the Zac1-enhanced cyclin D1 expression in human keratinocytes

Hung, Chih‐Tsung; Huang, Shih‐Ming; Cheng, Hsiao-Chun; Liu, Shuting; Chang, Yung‐Lung; Liu, Yingchun; Wang, Weiming

doi:10.1016/j.jdermsci.2015.06.006

Cited by 3 publications

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“…We have previously found that Zac1 enhances the expression of cyclin D1 and may promote the cell cycle progression. These findings indicated that Zac1 plays a dual role, modulating not only cell differentiation and apoptosis but also cell proliferation [ 30 , 31 ]. In previous experiments, we evidenced that curcumin inhibited Zac1-enhanced cyclin D1 expression in human keratinocytes and prevented the keratinocytes from entering the S phase in the cell cycle [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

The cytotoxic mechanism of epigallocatechin gallate on proliferative HaCaT keratinocytes

et al. 2017

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BackgroundEpigallocatechin gallate (EGCG) is the major ingredient of sinecatechins ointment, approved for the treatment of external genital and perianal warts. However, the molecular mechanism for EGCG’s effect on warts resulting from the human papillomavirus (HPV) infection of keratinocytes is not well understood. HPV may survive in proliferative keratinocytes and may be involved in cell cycle regulation and progression. The objective of this study was to investigate the mechanism underlying EGCG’s treatment on external genital warts of HPV infection through the cultured keratinocyte cells from the HaCaT cell line.MethodsMTT and flow cytometry assays were used to measure cell viability and the cell cycle profile, with and without EGCG treatment, for HaCaT keratinocyte cells cultured in a calcium-free medium and 1.8 mM calcium which induced proliferative and differentiated keratinocytes, respectively, for 24 h. The expression levels of cytotoxic proteins and factors were evaluated with the RT-PCR and western blotting analysis.ResultsEGCG influenced the proliferation stage but not the differentiation stage of keratinocytes. We suggest that apoptosis and autophagy might be the possible mechanism for the EGCG’s effect on the proliferative HaCaT cells. Furthermore, we found that EGCG reduced the protein levels of cyclin D1 and Zac1 (a zinc-finger protein which regulates apoptosis and cell cycle arrest 1) dose-dependently in proliferative as compared to differentiated keratinocytes. It also induced the expression of p21 and DEC1 (differentiated embryo-chondrocyte expressed gene 1), and promoted G1 arrest of cell cycle in proliferative keratinocytes.ConclusionsThese results help clarify the mechanisms of EGCG treatment of HPV-infected keratinocytes and may contribute to new targets, such as Zac1 and DEC1 for external genital and perianal warts.

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Section: Discussionmentioning

confidence: 99%

The cytotoxic mechanism of epigallocatechin gallate on proliferative HaCaT keratinocytes

et al. 2017

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“…Eleven in vitro studies ( Cho et al, 2007 ; Sun et al, 2012 ; Song et al, 2014 ; Esposito et al, 2015 ; Hung et al, 2015 ; Zhao et al, 2015 ; Varma et al, 2017 ; Wang WQ. et al, 2019 ; Wang ZJ.…”

Section: Resultsunclassified

“…Psoriasis related mechanisms in keratinocytes were induced using vascular endothelial growth factor ( Wang ZJ. et al, 2019 ; Zhang et al, 2020 ), IL-22 ( Zhao et al, 2015 ), IMQ ( Varma et al, 2017 ), TNF-α ( Cho et al, 2007 ; Sun et al, 2012 ; Yuyun et al, 2021 ), nanostructured lipid dispersions ( Esposito et al, 2015 ), and pSG5.HA.mZac1 ( Hung et al, 2015 ). Supplementary Tables S2, S3 summarize the characteristics of the included preclinical studies.…”

Section: Resultsmentioning

confidence: 99%

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Efficacy and safety of curcumin in psoriasis: preclinical and clinical evidence and possible mechanisms

et al. 2022

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Background: Psoriasis is a chronic and immune-mediated inflammatory skin disease. Many studies have shown that curcumin (CUR) has strong anti-inflammatory effects and can improve psoriasis; however, its efficacy and safety have not been confirmed, and the specific mechanism remains to be elucidated.Objective: To evaluate the efficacy, safety, and possible mechanisms of CUR in the treatment of psoriasis.Methods: The Cochrane Library, Embase, PubMed, Web of Science, China National Knowledge Infrastructure, Wanfang, and VIP (China Science and Technology Journal Database) were systematically searched for clinical trials and preclinical studies on the use of CUR in psoriasis treatment. All databases were searched from inception to January 2022. The meta-analysis was performed using RevMan 5.3 software.Results: Our meta-analysis included 26 studies, comprising seven clinical randomized controlled trials and 19 preclinical studies. A meta-analysis of clinical trials showed that both CUR monotherapy and combination therapy improved Psoriasis Area and Severity Index (PASI) scores in patients compared to controls (standard mean difference [std.MD]: −0.83%; 95% confidence interval [CI]: −1.53 to 0.14; p = 0.02). In preclinical studies, CUR showed better performance in improving the phenotype of psoriatic dermatitis mice compared to controls, including total PASI score (std.MD: 6.50%; 95% CI: 10.10 to −2.90; p = 0.0004); ear thickness (p = 0.01); and the expression of inflammatory cytokines such as interleukin (IL)-17, tumor necrosis factor (TNF)-α, IL-17F, and IL-22 (p < 0.05). In cell studies, CUR inhibited cell proliferation (p = 0.04) and the cell cycle (p = 0.03) and downregulated the inflammatory cytokines IL-6 and IL-8 (p < 0.05).Conclusions: CUR has excellent efficacy and broad potential to treat psoriasis in multiple ways. Its use also plays a crucial role in improving the psoriasis phenotype and reducing the inflammatory microenvironment. In conclusion, our findings suggest that CUR alone or in combination with other conventional treatments can effectively treat psoriasis.

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γ-Tocotrienol prevents cell cycle arrest in aged human fibroblast cells through p16INK4a pathway

et al. 2016

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Human diploid fibroblasts (HDFs) proliferation in culture has been used as a model of aging at the cellular level. Growth arrest is one of the most important mechanisms responsible for replicative senescence. Recent researches have been focusing on the function of vitamin E in modulating cellular signaling and gene expression. Therefore, the aim of this study was to elucidate the effect of palm γ-tocotrienol (vitamin E) in modulating cellular aging through p16 pathway in HDF cells. Primary culture of senescent HDFs was incubated with 70 μM of palm γ-tocotrienol for 24 hours. Silencing of p16 was carried out by siRNA transfection. RNA was extracted from the different treatment groups and gene expression analysis was carried out by real-time reverse transcription polymerase chain reaction. Proteins that were regulated by p16 were determined by western blot technique. The finding of this study showed that p16 mRNA was overexpressed in senescent HDFs, and hypophosphorylated-pRb and cyclin D1 protein expressions were increased (p < 0.05). However, downregulation of p16 and hypophosphorylated-pRb and cyclin D1 protein expressions (p < 0.05) by γ-tocotrienol led to modulation of the cell cycle regulation during cellular aging. In conclusion, senescent HDFs showed change in biological process specifically in cell cycle regulation with elevated expression of genes and proteins which may contribute to cell cycle arrest. Palm γ-tocotrienol may delay cellular senescence of HDFs by regulating cell cycle through downregulation of p16 and hypophosphorylated-pRb and cyclin D1 protein expressions.

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The inhibitory mechanism by curcumin on the Zac1-enhanced cyclin D1 expression in human keratinocytes

Cited by 3 publications

References 52 publications

The cytotoxic mechanism of epigallocatechin gallate on proliferative HaCaT keratinocytes

The cytotoxic mechanism of epigallocatechin gallate on proliferative HaCaT keratinocytes

Efficacy and safety of curcumin in psoriasis: preclinical and clinical evidence and possible mechanisms

γ-Tocotrienol prevents cell cycle arrest in aged human fibroblast cells through p16INK4a pathway

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