预约演示
更新于：2025-09-02
HDACs x VDR
更新于：2025-09-02
关联
NCT04400890
Randomized Double-Blind Placebo-Controlled Proof-of-Concept Trial of Resveratrol, a Plant Polyphenol, for the Outpatient Treatment of Mild Coronavirus Disease (COVID-19)
SLCTR/2018/019
Synergistic Effects of delta-Tocotrienol, Resveratrol and Vitamin D Supplementation on Modulation of Biochemical Markers, Cytokines and miRNAs in patients of type 2 diabetes mellitus
NCT01646567
A Double-Blind, Within-Subject Randomised, Placebo-Controlled, Proof of Concept, Comparison Study of SHP-141C Topical Cream in Psoriasis, Using the Microplaque Assay.
100 项与 HDACs x VDR 相关的临床结果
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100 项与 HDACs x VDR 相关的转化医学
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2025-10-01JOURNAL OF NUTRITIONAL BIOCHEMISTRY
1,25(OH)2D3 ameliorates DSS-induced intestinal ferroptosis through the SIRT3–SOD2–mtROS pathway
Article
作者: Ma, Xiao-Han ; He, Xue ; Zhu, Ya-Wen ; Wang, Hong-Qian ; Tong, Cheng-Cheng ; Chen, Xi ; Chen, Zhuo ; Guan, Jing ; Dou, Zi-Yue ; Xu, De-Xiang
Ferroptosis has been shown to play a significant role in the pathogenesis of ulcerative colitis (UC). This study investigated the effects of 1,25(OH)2D3 supplementation on ferroptosis in dextran sulfate sodium (DSS)-evoked colitis. Intestinal VDR was reduced in UC patients. Accordingly, GPX4 was downregulated and ACSL4 was upregulated in the intestine of UC patients. Animal experiments indicated that vitamin D deficiency exacerbated DSS-induced intestinal ferroptosis in mice. Conversely, pretreatment with 1,25(OH)2D3 alleviated DSS-induced ferroptosis in mouse intestine. Similarly, 1,25(OH)2D3 supplementation inhibited DSS-induced ferroptosis in HT-29 cells. Furthermore, we found decreased intestinal SIRT3 protein and increased acetylated superoxide dismutase 2 (Ac-SOD2) in UC patients. Pretreatment with 1,25(OH)2D3 attenuated DSS-induced downregulation of SIRT3 and acetylation of SOD2 in both mouse intestine and HT-29 cells. Moreover, 1,25(OH)2D3 pretreatment inhibited mitochondrial reactive oxygen species (mtROS) in DSS-treated HT-29 cells. Finally, transfection with SIRT3 siRNA antagonized the protective effect of 1,25(OH)2D3 on ferroptosis in DSS-treated HT-29 cells. Overall, our results suggest that 1,25(OH)2D3 alleviates DSS-induced intestinal ferroptosis via the SIRT3-SOD2-mtROS pathway, further supporting the potential use of 1,25(OH)2D3 supplementation in UC treatment.
2025-09-01BIOMEDICINE & PHARMACOTHERAPY
Vitamin D and SIRT1 activator SRT2104 cooperate in antiproliferative activity in lung cancer through ferroptosis induction
Article
作者: Totoń-Żurańska, Justyna ; Lewoń-Mrozek, Dominika ; Wietrzyk, Joanna ; Maj, Ewa ; Bobak, Klaudia ; Ledwoń, Anna
A number of studies showed that vitamin D reveals antiproliferative activity against cancer cells, however some lung cancer cells are more sensitive than others. Secondly, there are some controversies around the role of SIRT1 in lung cancer: on one hand it was demonstrated that SIRT1 contributed to the development of lung cancer, on the other hand SIRT1 was showed to be downregulated in lung cancer. Third, it was demonstrated that VDR is posttranslationally modified via deacetylation by SIRT1 what potentiated VDR activity. In this study, we first showed an inverse correlation between VDR and SIRT1 expression level in lung cancer. We further revealed that vitamin D and SIRT1 activator SRT2104 cooperate in inhibiting lung cancer cells proliferation. SRT2104 enhanced transcriptional activity of calcitriol in lung cancer cells, since the expression of CYP24A1 was significantly higher after the treatment with calcitriol and SRT2104 compared with calcitriol alone. Calcitriol and SRT2104 affected the metabolic rate of lung cancer cells, increased ROS and superoxide production, decreased GSH/GSSG ratio and induced lipid peroxidation. Calcitriol and SRT2104 also significantly induced the expression of COX-2 and reduced the level of Hsp90 and mutp53 in EGFR mutant lung cancer cells. The study showed that the use of calcitriol in combination with SRT2104 SIRT1 activator shows stronger antitumor activity in lung cancer. This effect may be due to the induction of ferroptosis. These insights pave the way for potential to use SIRT1 activators with vitamin D derivatives in the treatment of lung cancer.
2025-08-01MEDICINE
Roles of JUN and MMP1 in lung cancer brain metastases
Article
作者: Sun, Cai-Xing ; Xia, Liang ; Wu, Bin ; Jing, Kai ; Zou, Yang-Fan ; Zhang, Shu-Yuan ; Wang, Lei ; Li, Li-Weng
Lung cancer brain metastases refer to intracranial space-occupying lesions formed by the metastasis of tumor cells from the lung to the brain parenchyma or dissemination in the meninges. The datasets GSE200563 and GSE126548 for lung cancer brain metastasis were obtained from gene expression omnibus database with the platform files GPL21697 and GPL16791. Differentially expressed genes analysis was conducted, followed by weighted gene co-expression network analysis, construction and analysis of protein–protein interaction networks, functional enrichment analysis, gene set enrichment analysis, comparative toxicogenomics database analysis. Five hundred differentially expressed genes were identified. According to gene ontology, they were mainly enriched in terms of fucosyltransferase activity, protein–DNA complex, cAMP signaling pathway, and transcriptional misregulation in cancer. Ten core genes (JUN, IL1A, VEGFA, MMP1, EDN1, SOCS3, NOD2, NCOR2, VDR, and HDAC2) were obtained. Comparative toxicogenomics database analysis revealed associations between core genes (JUN, IL1A, VEGFA, MMP1, EDN1, SOCS3, NOD2, NCOR2, VDR, and HDAC2) and tumor cell transformation, non-small cell carcinoma, lung neoplasms, tumor invasiveness, tumor metastasis, and inflammation. JUN and MMP1 are abnormally highly expressed in lung cancer brain metastasis tissues, which may be their molecular targets.
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