Low Trichorhinophalangeal Syndrome 1 Gene Transcript Levels in Basal-like Breast Cancer Associate with Mesenchymal-to-epithelial Transition

Regardless of advances in detection and treatment, breast cancer affects about 1.5 million women all over the world. Since the last decade, genome-wide association studies (GWAS) have been extensively conducted for breast cancer to define the role of miRNA as a tool for diagnosis, prognosis and therapeutics. MicroRNAs are small, non-coding RNAs that are associated with the regulation of key cellular processes such as cell multiplication, differentiation, and death. They cause a disturbance in the cell physiology by interfering directly with the translation and stability of a targeted gene transcript. MicroRNAs (miRNAs) constitute a large family of non-coding RNAs, which regulate target gene expression and protein levels that affect several human diseases and are suggested as the novel markers or therapeutic targets, including breast cancer. MicroRNA (miRNA) alterations are not only associated with metastasis, tumor genesis but also used as biomarkers for breast cancer diagnosis or prognosis. These are explained in detail in the following review. This review will also provide an impetus to study the role of microRNAs in breast cancer.

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Enantioselective Effect of Flutriafol on Growth, Deoxynivalenol Production, and TRI Gene Transcript Levels in Fusarium graminearum

Journal of Agricultural and Food Chemistry ◽

10.1021/acs.jafc.0c06800 ◽

2021 ◽

Vol 69 (5) ◽

pp. 1684-1692

Author(s):

Chaofeng Li ◽

Shuai Fan ◽

Yan Wen ◽

Zhenchao Tan ◽

Chenglan Liu

Keyword(s):

Fusarium Graminearum ◽

Gene Transcript ◽

Transcript Levels

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FOXC1 Activates Smoothened-Independent Hedgehog Signaling in Basal-like Breast Cancer

Cell Reports ◽

10.1016/j.celrep.2015.09.063 ◽

2015 ◽

Vol 13 (5) ◽

pp. 1046-1058 ◽

Cited By ~ 71

Author(s):

Bingchen Han ◽

Ying Qu ◽

Yanli Jin ◽

Yi Yu ◽

Nan Deng ◽

...

Keyword(s):

Breast Cancer ◽

Hedgehog Signaling ◽

Basal Like Breast Cancer

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Expression of human endogenous retrovirus-K is strongly associated with the basal-like breast cancer phenotype

Scientific Reports ◽

10.1038/srep41960 ◽

2017 ◽

Vol 7 (1) ◽

Cited By ~ 32

Author(s):

Gary L. Johanning ◽

Gabriel G. Malouf ◽

Xiaofeng Zheng ◽

Francisco J. Esteva ◽

John N. Weinstein ◽

...

Keyword(s):

Breast Cancer ◽

Endogenous Retrovirus ◽

Human Endogenous Retrovirus ◽

Basal Like Breast Cancer ◽

Cancer Phenotype

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Cross-generational feeding of Bt (Bacillus thuringiensis)-maize to zebrafish (Danio rerio) showed no adverse effects on the parental or offspring generations

British Journal Of Nutrition ◽

10.1017/s0007114513001748 ◽

2013 ◽

Vol 110 (12) ◽

pp. 2222-2233 ◽

Cited By ~ 6

Author(s):

Monica Sanden ◽

Robin Ornsrud ◽

Nini H. Sissener ◽

Susanne Jorgensen ◽

Jinni Gu ◽

...

Keyword(s):

Bacillus Thuringiensis ◽

Danio Rerio ◽

Fumonisin B1 ◽

Gene Transcript ◽

Transcript Levels ◽

Two Generations ◽

Feed Utilisation ◽

Liver Gene ◽

Caspase 6 ◽

Mass Increase

In the present study, zebrafish (Danio rerio) were fed casein/gelatin-based diets containing either 19 % Bt (Bacillus thuringiensis)-maize or its parental non-Bt (nBt)-maize control for two generations (F0: sixty fish; F1: forty-two to seventy fish per treatment). The study focused on growth and reproductive performance, liver CuZn superoxide dismutase (SOD) enzyme activity, gene transcript levels targeting important cellular pathways in the liver and mid-intestine, histomorphological evaluation of the intestine, differential leucocyte counts, offspring larva swimming activity and global DNA methylation in offspring embryos. No significant effects were observed in the parental generation. The offspring were either fed the same diets as those fed to their parents (Bt–Bt or nBt–nBt) or switched from the Bt diet to the nBt diet (Bt–nBt). The Bt–Bt offspring exhibited a significantly higher body mass increase, specific growth rate and feed utilisation than fish fed the nBt–nBt diet and/or fish fed the Bt–nBt diet. Liver and mid-intestinal gene transcript levels of CuZn SOD were significantly higher in fish fed the nBt–nBt diet than in those fed the Bt–Bt diet. Liver gene transcript levels of caspase 6 were significantly lower for the nBt–nBt group than for the Bt–Bt group. Overall, enhanced growth performance was observed in fish fed the Bt diet for two generations than in those fed the nBt diet for one and two generations. Effects observed on gene biomarkers for oxidative stress and the cell cycle (apoptosis) may be related to the contamination of nBt-maize with fumonisin B1 and aflatoxin B1. In conclusion, it is suggested that Bt-maize is as safe and nutritious as its nBt control when fed to zebrafish for two generations.

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Migrations of cancer cells through the lens of phylogenetic biogeography

Scientific Reports ◽

10.1038/s41598-021-96215-9 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Antonia Chroni ◽

Sayaka Miura ◽

Olumide Oladeinde ◽

Vivian Aly ◽

Sudhir Kumar

Keyword(s):

Breast Cancer ◽

Cell Migration ◽

Molecular Evolution ◽

Simulated Data ◽

Malignant Cells ◽

Founder Effects ◽

Initial Tumor ◽

Variation Data ◽

Basal Like Breast Cancer ◽

Tumor Genome

AbstractMalignant cells leave their initial tumor of growth and disperse to other tissues to form metastases. Dispersals also occur in nature when individuals in a population migrate from their area of origin to colonize other habitats. In cancer, phylogenetic biogeography is concerned with the source and trajectory of cell movements. We examine the suitability of primary features of organismal biogeography, including genetic diversification, dispersal, extinction, vicariance, and founder effects, to describe and reconstruct clone migration events among tumors. We used computer-simulated data to compare fits of seven biogeographic models and evaluate models’ performance in clone migration reconstruction. Models considering founder effects and dispersals were often better fit for the clone phylogenetic patterns, especially for polyclonal seeding and reseeding of metastases. However, simpler biogeographic models produced more accurate estimates of cell migration histories. Analyses of empirical datasets of basal-like breast cancer had model fits consistent with the patterns seen in the analysis of computer-simulated datasets. Our analyses reveal the powers and pitfalls of biogeographic models for modeling and inferring clone migration histories using tumor genome variation data. We conclude that the principles of molecular evolution and organismal biogeography are useful in these endeavors but that the available models and methods need to be applied judiciously.

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Abstract 15: Glucose-Mediated Remodeling of Cardiac DNA Methylation

Circulation Research ◽

10.1161/res.121.suppl_1.15 ◽

2017 ◽

Vol 121 (suppl_1) ◽

Author(s):

Mark E Pepin ◽

David K Crossman ◽

Joseph P Barchue ◽

Salpy V Pamboukian ◽

Steven M Pogwizd ◽

...

Keyword(s):

Gene Expression ◽

Heart Failure ◽

Dna Methylation ◽

Diabetic Cardiomyopathy ◽

Left Ventricular ◽

Epigenetic Mark ◽

Gene Transcript ◽

Transcript Levels ◽

Glycemic Memory

To identify the role of glucose in the development of diabetic cardiomyopathy, we had directly assessed glucose delivery to the intact heart on alterations of DNA methylation and gene expression using both an inducible heart-specific transgene (glucose transporter 4; mG4H) and streptozotocin-induced diabetes (STZ) mouse models. We aimed to determine whether long-lasting diabetic complications arise from prior transient exposure to hyperglycemia via a process termed “glycemic memory.” We had identified DNA methylation changes associated with significant gene expression regulation. Comparing our results from STZ, mG4H, and the modifications which persist following transgene silencing, we now provide evidence for cardiac DNA methylation as a persistent epigenetic mark contributing to glycemic memory. To begin to determine which changes contribute to human heart failure, we measured both RNA transcript levels and whole-genome DNA methylation in heart failure biopsy samples (n = 12) from male patients collected at left ventricular assist device placement using RNA-sequencing and Methylation450 assay, respectively. We hypothesized that epigenetic changes such as DNA methylation distinguish between heart failure etiologies. Our findings demonstrated that type 2 diabetic heart failure patients (n = 6) had an overall signature of hypomethylation, whereas patients listed as ischemic (n = 5) had a distinct hypermethylation signature for regulated transcripts. The focus of this initial analysis was on promoter-associated CpG islands with inverse changes in gene transcript levels, from which diabetes (14 genes; e.g. IGFBP4) and ischemic (12 genes; e.g. PFKFB3) specific targets emerged with significant regulation of both measures. By combining our mouse and human molecular analyses, we provide evidence that diabetes mellitus governs direct regulation of cellular function by DNA methylation and the corresponding gene expression in diabetic mouse and human hearts. Importantly, many of the changes seen in either mouse type 1 diabetes or human type 2 diabetes were similar supporting a consistent mechanism of regulation. These studies are some of the first steps at defining mechanisms of epigenetic regulation in diabetic cardiomyopathy.

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