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2 edition of effects of folate deficiency on gene expression in human colorectal adenocarcinoma cell lines. found in the catalog.

effects of folate deficiency on gene expression in human colorectal adenocarcinoma cell lines.

Petar Novakovic

effects of folate deficiency on gene expression in human colorectal adenocarcinoma cell lines.

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Published .
Written in English


About the Edition

Folate is a B vitamin that inversely modulates colorectal carcinogenesis. Folate status is also an important determinant in chemotherapeutic response. Mediating the transfer of one-carbon moieties is the sole biochemical function known for folate, and in this role folate plays a critical role in DNA synthesis, repair and methylation. In vitro models of folate deficiency were used to determine the effects of folate deficiency on gene expression in several human colorectal cancer cell lines. Folate deficiency altered the expression patterns of genes found to be involved in metabolism, intracellular signalling, cell cycle, DNA repair, transcriptional regulation, angiogenesis, cell adhesion, transport, and cytoskeletal organization and microtubule-based movement, in a cell-specific manner. These studies provide insight into the specific molecular targets of folate deficiency, and therefore will allow for a better understanding of the mechanism of action associated with the folate depletion-enhanced cytotoxicity on cancer cells.

The Physical Object
Pagination181 leaves.
Number of Pages181
ID Numbers
Open LibraryOL19217481M
ISBN 100494074329

  Given that several targeted therapies directed towards folate receptor alpha (FRA) are in late stage clinical development, the sensitive and robust detection of FRA in tissues is of paramount importance relative to patient selection, prognosis and prediction. In the present study we undertook an immunohistochemical evaluation of expression of FRA in breast cancer samples using formalin-fixed Cited by: Several lines of evidence, both in vitro and in vivo, suggest that folate deficiency has pro-neoplastic effects. Deoxynucletide pool imbalance and uracil misincorporation into DNA in folate deficient cell lines has been described. Enhanced development of colonic neoplasia was observed in a . Dr. Doni Wilson, author of The Stress Remedy, explains how health issues such as anxiety, migraines and high blood pressure could be caused by a genetic mutation.. I hear from so many patients who have fatigue, irritability, brain fog, anxiety, sleep issues, and/or . SCE in embryo and cell lines: Studies demonstrating beneficial effects of folate on critical colorectal cancer endpoints: Rat M. Izumi, and T. A. Graubert, “The impact of copy number variation on local gene expression in mouse hematopoietic stem and progenitor cells,” Nature Genetics, vol. 41, no. 4, Cited by: 6.


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effects of folate deficiency on gene expression in human colorectal adenocarcinoma cell lines. by Petar Novakovic Download PDF EPUB FB2

We therefore investigated the effects of folate depletion on expression of genes involved in apoptosis and cancer pathways in four human colon adenocarcinoma cell lines in an in vitro model of folate deficiency.

Apoptosis and cancer pathway-specific mini-microarray were used to screen for differentially expressed genes in response to folate Cited by: We therefore investigated the effects of folate depletion on expression of genes involved in apoptosis and cancer pathways in four human colon adenocarcinoma cell lines in an in vitro model of.

Folic acid treatment of cell lines. The three human cell lines used in this study were chosen for their differences in phenotype. The non-transformed MCF10A cells acted as a non-tumorigenic control, while MCF7 and HsT cells represented ER-positive and PR-positive, and triple-negative breast adenocarcinoma tumours, by: 5.

The portfolio of evidence from animal, human, and in vitro studies suggests that the effects of folate deficiency on DNA methylation are highly complex; appear to Author: Young-In Kim.

Folate deficiency is also associated with an increased risk of certain types of cancer (17, 18). In addition, FB 1 inhibits the FR and consequently blocks folate internalization in Caco-2, a human colon adenocarcinoma cell line (19). The effect of FB 1 on folate transport in hepatocarcinoma has not been yet by:   Folate metabolism, DNA methylation and dna synthesis.

Folate is a generic term for a naturally occurring family of B-group vitamins composed of an aromatic pteridine ring linked to p-aminobenzoic acid and a glutamate residue (Shane, ).Following absorption in the small intestine dietary food folates undergo hydrolysis to methyltetrahydrofolate (methylTHF), the predominant form Cited by: 1.

Introduction. Inthe US government mandated synthetic folic acid (FA) supplementation of breakfast cereals and grains, to alleviate the FA deficiency that was causing the increased incidence of neural tube defects (NTDs) in then, the occurrence of human neural tube defects has reportedly decreased by 35–75%.FA, also referred to as vitamin B9, is a water Cited by: Changes in expression may explain the inverse relationship observed between folate status and risk of colorectal cancer.

Three cell lines derived from the normal human colon, HCEC, NCM and NCM, were grown for 32–34 days in media contain 50, 75 or nM folic acid, and the expression of genes involved in cell-cycle checkpoints Cited by: colorectal cancer.

Three cell lines derived from the normal human colon, HCEC, NCM and NCM, were grown for 32–34 days in media contain 50, 75 or nM folic acid, and the expression of genes involved in cell-cycle checkpoints, intracellular signaling, folate uptake and cell adhesion and migration was determined.

For the assessment of folate-based radiopharmaceuticals, human nasopharyngeal KB carcinoma cells are traditionally used although nasopharyngeal cancer is rare.

On the other hand, the folate receptor (FR) is frequently overexpressed on diverse cancer types, the highest frequency (>90%) being on ovarian carcinomas. The goal of our study was the in vitro and in vivo assessment of Cited by: RNA cell line category i The cell lines in the Human Protein Atlas have been analyzed by RNA-seq to estimate the transcript abundance of each protein-coding gene.

The RNA-seq data was then used to classify all genes according to their cell line-specific expression into one of six different categories, defined based on the total set of all NX.

Folate is an essential member of the vitamin B complex family that is naturally present in grains, green leafy vegetables, and liver. Folic acid and the L-methylfolate (5-MTHF) derivative are synthetic supplemental forms that have higher is important in cell growth and division and involved in the methylation process and DNA synthesis.

Whether Folic acid is a potential drug that may prevent the progression of colorectal carcinoma and when to use are important healthy issues we focus on. Our study is to examine the effect of folic acid on the development of the CRC and the optimal time folic acid should be provided in a mouse-ICR model induced by 1, 2-Dimethylhydrazine.

Also, we investigated the gene expression Cited by:   The gene is key to the normal progression of the folic acid cycle and, when mutated, it results in abnormal folic acid metabolism causing similar effects to dietary folic acid deficiency.

Folate has a central role in the cell metabolism. This study aims to explore the DNA methylation pattern of the folate transporter genes FOLR1, PCFT, and RFC1 as well as the corresponding protein expressions in colorectal cancer (CRC) tissue and adjacent non-cancerous mucosa (ANCM).

Our results showed statistically significant differences in the DNA-methylated Cited by: 4. fluorescent folate targeted agent, FolateRSense.

(FR), and used it to noninvasively quantify FR expression in vivo by FMT of mouse tumor xenografts. Three different cell types, KB, HeLa and HT, with varying degrees of FR expression were employed in the present studies. In vitro, the binding of FolateRSense to each.

Effect of Folate on Colon and Blood Cells. Measurements of differential gene expression in colonic and blood cells by microarray analysis, further defining folate's action in modifying cell cycle activity, cell maturation, signal transduction and oncogene expression.

adenocarcinoma in a mouse model of colorectal cancer: microarray gene expression profile Yan-Wei Lin†, Ji-Lin Wang†, Hui-Min Chen, Yan-Jie Zhang, Rong-Lu, Lin-Lin Ren, Jie Hong* and Jing-Yuan Fang* Abstract Background: Whether Folic acid is a potential drug that may prevent the progression of colorectal carcinoma andCited by:   The FOLR1 gene provides instructions for making a protein called folate receptor alpha.

This protein helps regulate transport of the B-vitamin folate into cells. Folate (also called vitamin B9) is needed for many processes, including the production and repair of DNA, regulation of gene activity (expression), and protein production.

Expression of Folate Receptor alpha and its Clinical Significance in Breast Cancer Folate deficiency - Duration: Cell Signaling- Tyrosine Kinase receptors - Duration. Recently, several studies of global gene expression patterns in human tumors and tumor cell lines have been published (Perou et al.,; Alizadeh et al., ; Ross et al., ).

Each of these studies identified a prominent cluster of genes whose expression was correlated with the rate of proliferation of the tumors or cell lines under.

Abstract: While conventional therapies have improved the outcome for patients with ovarian cancer, the disease still accounts for the most gynecological cancer-related deaths.

The development of new treatment options is needed and efforts have focused on targeted therapies which aim to improve patient outcome by increasing anti-tumor activity while minimizing toxicity. Numerous studies have investigated the effects of folic acid supplementation on colorectal cancer risk, but conflicting results were reported.

We herein performed a Cited by:   Chronic mild folate depletion affects prostate cells' phenotype. We grew three syngenic, but phenotypically distinct, clonal cell lines; C-2D (benign), C-2G (tumourigenic) and C-2H (metastatic), which were generated from a primary prostate tumour in a TRAMP mouse [], in folate-restricted ( nM) medium for 20 PD and refer to these cells as D, G, and H, by: Hereditary folate malabsorption (HFM) is a rare autosomal recessive disorder caused by loss-of-function mutations in the proton-coupled folate transporter (PCFT) gene, resulting in systemic folate deficiency and impaired delivery of folate to the brainSpecialty: Medical genetics.

Grant Number: 5U54CA PI Name: HUNTER Project Title: Folate, 1-Carbon Nutrients, Gene Variants & Colon Cancer Abstract: DESCRIPTION (provided by applicant): Most of the over twenty epidemiologic studies that have examined the relationship between dietary folate intake and the risk of developing colorectal neoplasms, have reported that higher folate intakes are associated with lower risk.

Using prostate cancer cell lines Hsu et al. showed that sulforaphane down regulated the expression of both DNMT1 and -3b, leading to demethylation of the CCND2 promoter and restoration of gene expression. CCND2 is a regulator of cell cycle and can thereby exert anti-cancer by: Colorectal cancer (CRC) is a heterogeneous disease that includes both hereditary and sporadic types of tumors.

Tumor initiation and growth is driven by mutational or epigenetic changes that alter the function or expression of multiple genes. The genes predominantly encode components of various intracellular signaling cascades.

In this review, we present mouse intestinal cancer models that Author: Monika Stastna, Lucie Janeckova, Dusan Hrckulak, Vitezslav Kriz, Vladimir Korinek. Grant Number: 5R01CA PI Name: Conti Project Title: Incorporating intermediate biomarkers of folate with colorectal cancer Abstract: DESCRIPTION (provided by applicant): "Incorporating intermediate biomarkers of folate with colorectal cancer" The goal of this proposal is to measure intermediate biomarkers and to evaluate these with statistical methods designed to elucidate the.

The new study, published in the March 15 issue of the journal Cancer Research (), provides evidence that a combination of folate deficiency. Intake of high levels of folate may reduce colorectal cancer risk, according to a new study.

Folate is a water-soluble B vitamin that occurs naturally in food. Folate targeting is a method utilized in biotechnology for drug delivery purposes. This Trojan Horse process, which was created by Drs.

Christopher P. Leamon and Philip S. Low, involves the attachment of the vitamin, folate (), to a molecule/drug to form a "folate conjugate". Based on the natural high affinity of folate for the folate receptor protein (FR), which is commonly expressed on the. Altered folate availability modifies the molecular environment of the human colon: implications for colorectal carcinogenesis Petr Protiva*,1,2,3, Joel B Mason*,4, Zhenhua Liu4, Michael E Hopkins1, Celeste Nelson1, James R Marshall5, Richard W.

Lambrecht3, Swaroop Pendyala1, Levy Kopelovich6, Myungjin Kim7,§, Steven H. Kleinstein8, Peter W Laird7, Martin Lipkin9, and Peter R Holt1,†. The clinical syndrome due to mismatch repair gene deficiency is known as Hereditary Non-Polyposis Colorectal Cancer (HNPCC) and accounts for 2–5% of all colorectal cancer cases.

Affected kindreds have an unusually high occurrence of colorectal and certain. The gene mutation MTHFR and its role in cancer. Date. Updated Septem A key component of methylating processes that occur within every cell of the human body is the gene MTHFR (methylenetetrahydrofolate reductase).

Both folate and one-carbon metabolism are reliant on the MTHFR gene. METHOD: The global gene expression profile was identified and analyzed using the Affymetrix HG-U Plus array. RESULTS: There was a significant dysregulation in the global gene expression of the FOLR1-suppressed taxol-resistant nasopharyngeal carcinoma cell lines.

There were 41 upregulated genes and downregulated genes. Lacey et al. () constructed a cDNA library from a human carcinoma cell line that abundantly expressed the membrane form of the folate receptor. A nearly full-length cDNA for the folate binder was isolated.

The deduced amino acid sequence was not consistent with a typical membrane-spanning domain, but rather with a signal for anchoring via a glycosyl-phosphatidylinositol linkage. Proposed Mechanisms for the Effects of Folate and Methionine on Intestinal Tumour Growth in ApcMin/+ Mice 35 Modulation of Nucleotide Synthesis Caused by Folate Deficiency or Excess 36 DNA Methylation Changes Due to Deficiency of Methyl Donors Which May.

June 5, -- Popular folic acid supplements fail to protect against colon cancer, but they may increase an adult's risk of other cancers.

Animal studies led researchers to think that folic Author: Daniel J. Denoon. Although the primary risk factors for developing oral cancers are well understood, less is known about the relationship among the secondary factors that may modulate the progression of oral cancers, such as high-risk human papillomavirus (HPV) infection and folic acid (FA) supplementation.

This study examined high-risk HPV and FA supplementation effects, both singly and in combination, Cited by: 3. Colorectal cancer is the second leading cause of cancer-related death in the Western industrialized world.

Many epidemiological studies have shown a negative association between colorectal cancer incidence and vitamin D levels. It has been suggested that the antitumoral action of 1,25(OH)2D3 in colorectal cancer relies on several mechanisms at the cellular : Argjira Juniku-Shkololli.Folate receptor alpha (FRA) is a cell-surface glycoprotein responsible for the transport of folate across cell membranes.

FRA has demonstrated restricted expression in polarized epithelial cells in a subset of normal tissues, as well as certain cancers of epithelial origin. FRA expressionFile Size: 1MB. Dietary folate appears to be inversely related to colorectal cancer risk. This study investigated the effects of dietary intervention with folate on the development of intestinal polyps in Min (Apc+/−) mice.

Weanling Min mice were fed diets containing 0, 2 (basal requirement), 8, or 20 mg folate/kg diet. At 3 and 6 months of dietary intervention, 50% of the mice from each group were Cited by: