Supplementary Figure 4 from Infiltrating Macrophages Induce ERα Expression through an IL17A-mediated Epigenetic Mechanism to Sensitize Endometrial Cancer Cells to Estrogen
Chengcheng NingBingying XieLin ZhangChunsheng LiWeiwei ShanBingyi YangXuezhen LuoChao GuQizhi HeHongyan JinXiaojun ChenZhenbo ZhangYouji Feng
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<p>IL-17 receptor antibody compromises the effect of IL-17A on ERα transcription up-regulation</p>RNA-Directed DNA Methylation
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Purpose: Endometrial cancer is a very common type of cancer in females worldwide. Advances in diagnosis and treatment have not decreased the incidence of endometrial cancer. Lately, research has been focused on revealing the molecular and genetic characteristics of endometrial cancer in order to provide new insights in the biology of this entity, leading hopefully to innovating therapies. Research has revealed that epigenetic modifications govern endometrial carcinogenesis. In this review, the epigenetic mechanisms that are involved in endometrial cancer as well as the differences between the different types of endometrial cancer are discussed. The review also refers to the putative therapeutic benefits that hopefully can arise.
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Inheritance
Non-Mendelian inheritance
Calorie Restriction
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SummaryAge-related clonal haemopoiesis (ARCH) in healthy individuals was initially observed through an increased skewing in X-chromosome inactivation [1]. More recently, several groups reported that ARCH is driven by somatic mutations [2], with the most prevalent ARCH mutations being in the DNMT3A and TET2 genes, previously described as drivers of myeloid malignancies. ARCH is associated with an increased risk for haematological cancers [2]. ARCH also confers an increased risk for non-haematological diseases, such as cardiovascular disease, atherosclerosis, and chronic ischemic heart failure, for which age is a main risk factor [3,4]. Whether ARCH is linked to accelerated ageing has remained unexplored. The most accurate and commonly used tools to measure age acceleration are epigenetic clocks: they are based on age-related methylation differences at specific CpG sites [5]. Deviations from chronological age towards an increased epigenetic age have been associated with increased risk of earlier mortality and age-related morbidities [5,6]. Here we present evidence of accelerated epigenetic age in individuals with ARCH.
Epigenesis
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Abstract The new complexes (III) decompose in the solid state or in solution on thermolysis to give ethane and cis‐PtMe2L2.
Energetics
Reductive elimination
Elimination reaction
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Estrogen plays an essential role in type I endometrial cancer cell proliferation. Despite great progresses in the etiology has been obtained in the past, however, the molecular mechanisms remain to be fully clarified. Prohibitin has been demonstrated involvement in multiple cancers' development. If it also contributes to estrogen-driven endometrial cancer proliferation is not clear. IHC assay result display that prohibitin overexpressed in endometrial cancer tissue and associated with the poor prognosis; Western blot assay detect that upregulated prohibitin expression with dose- and time-dependent manners. The cellular growth was monitored with SRB assay which demonstrate that knockdown prohibitin attenuated estrogen-induced proliferation. Ubiquitination assay finds estrogen increased prohibitin level through stabilizing prohibitin protein via inhibition of ubiquitination, while estrogen-induced protein expression was mediated by estrogen receptor. Our findings provide a new insight on the mechanism of estrogen-induced proliferation, implying the possibility of using prohibitin as a potential therapeutic target for the treatment of endometrial cancer.
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Endometrial cancer is the most commonly diagnosed gynaecological cancer. Based on differences in clinic pathologic characteristics, there are two subtypes of endometrial carcinoma Type 1 and Type 2. Multiple risk factors (Obesity, use of an intrauterine device, Age, Diet and Exercise, Type 2 Diabetes) are developing endometrial cancer. Likewise, epigenetics is the study of alteration gene and modulated gene expression with alteration in DNA sequences. In mammals, epigenetic modifications include DNA methylation, histone modifications, and miRNA.
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AbstractThe discovery of a family of highly conserved DNA cytosine methylases in honey bees and other insects suggests that, like mammals, invertebrates possess a mechanism for storing epigenetic information that controls heritable states of gene expression. Recent data also show that silencing DNA methylation in young larvae mimics the effects of nutrition on early developmental processes that determine the reproductive fate of honey bee females. We evaluate the impact of these findings on future studies of environmentally-driven phenotypic plasticity in social insects, and discuss how they may help in understanding the nutritional basis of epigenetic reprogramming in humans.
Reprogramming
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