- Research Associate Professor, Nutritional Sciences
- Associate, Center for Toxicology
- Ph.D. Molecular and Cellular Biology
- University of Padova, Padova, Italy
- Characterization of Anchorin II, a New Collagen Type II Receptor and Cellular Expression of Tropoelastin in the Developing Chick.
- University of Arizona, Arizona (2009 - 2011)
- University of Arizona, Arizona (2002 - 2009)
- University of Arizona, Arizona (1996 - 2002)
- NIEHS, NIH (1993 - 1996)
- VPI &SU (1990 - 1993)
My training and research background are in the field of molecular and developmental biology. My research activities have focused on the role of exposure to environmental and dietary factors in the etiology of developmental and chronic diseases including inflammation and cancer. Specific research objectives have been 1) to identify the molecular mechanisms through which ubiquitous environmental pollutants induce congenital heart disease; 2) elucidating the signaling pathways through which dietary agents influence epigenetic regulation of proinflammatory and tumor suppressor genes such as the breast cancer-1 (BRCA-1) and cyclooxygenase-2 (COX-2) genes. As a principal investigator at The University of Arizona I have been responsible for more than a decade for the acquisition and administration of research funds, recruitment and training of laboratory personnel and students, and delivery of scientific and administrative reports including research manuscripts, presentation at conferences, annual and progress reports. As a Faculty of the University of Arizona I have contributed to interdisciplinary programs, development of multi-principal investigators grants, and cross-training of staff and students.
Mediterranean Diet and HealthNutrition and Cancer Prevention/DevelopmentEpigenetic regulation in breast and colon cancer development
No activities entered.
- Selmin, O. (2018). Mediterranean diet for the prevention of er-negative breast cancers: Molecular interactions of olive oil and vegetable bioactives in HER2-enriched and TNBC. In Molecular Nutrition: Cancer. Andrew Neilson and Eva Schmelz, Editors.
- Selmin, O. (2018). Prevention of breast cancer by food bioactives in relation to cancer subtypes; Epigenetic mechanisms.. In Epigenetics of Chemoprevention: Bishayee A, Editor.
- Selmin, O. (2017). Nutritional epigenetics of nuclear receptors in breast cancer.. In Handbook of Nutrition.. Elsevier.
- Selmin, O. I., Runyan, R. B., & Makwana, O. (2014). Environmental Sensitivity to Trichloroethylene (TCE) in the Developing Heart. In Trichloroethylene: Toxicity and Health Risks(pp 153-169). London: Springer.
- Selmin, O. (2019). Arsenic-induced BRCA1 CpG promoter methylation is associated with the downregulation of ERα and resistance to tamoxifen in MCF7 breast cancer cells and mouse mammary tumor xenografts. International Journal of Oncology.
- Selmin, O. (2019). Dietary fat and obesity as modulators of BC risk: Focus on DNA methylation.. British Journal of Pharmacology. doi:doi: 10.1111/bph.14891.
- Selmin, O. (2019). Epigenetic Activation of BRCA1 by Genistein In Vivo and Triple Negative Breast Cancer Cells Linked to Antagonism toward Aryl Hydrocarbon Receptor. Nutrients, 11(11).
- Selmin, O. (2019). n-6 Linoleic Acid Induces Epigenetics Alterations Associated with Colonic Inflammation and Cancer.. Nutrients, 11(1).
- Selmin, O. (2018). Arsenic-induced BRCA1 CpG promoter methylation associates with down regulation of ERalpha and resistance to tamoxifen... International Journal of Oncology.
- Selmin, O. (2018). Aryl Hydrocarbon Receptor Diet and Breast Cancer Risk. The Yale Journal of Biology and Medicine.
- Selmin, O. (2018). n-6 linoleic acid induces epigenetic alterations associated with colonic inflammation and cancer. Nutrients.
- Runyan, R. B., Selmin, O. I., Lencinas, A., Nunez, M., Ismail, K. A., & Harris, A. P. (2018). Trichloroethylene perturbs HNF4a expression and activity in the developing chick heart. Toxicology Letters, 285(March 15), 113-120. doi:10.1016/j.toxlet.2017.12.027More infoExposure to trichloroethylene (TCE) is linked to formation of congenital heart defects in humans and animals. Prior interactome analysis identified the transcription factor, Hepatocyte Nuclear Factor 4 alpha (HNF4a), as a potential target of TCE exposure. As a role for HNF4a is unknown in the heart, we examined developing avian hearts for HNF4a expression and for sensitivity to TCE and the HNF4a agonist, Benfluorex. In vitro analysis using a HNF4a reporter construct showed both TCE and HFN4a to be antagonists of HNF4a-mediated transcription at the concentrations tested. HNF4a mRNA is expressed transiently in the embryonic heart during valve formation and cardiac development. Embryos were examined for altered gene expression in the presence of TCE or Benfluorex. TCE altered expression of selected mRNAs including HNF4a, TRAF6 and CYP2C45. There was a transition between inhibition and induction of marker gene expression in embryos as TCE concentration increased. Benfluorex was largely inhibitory to selected markers. Echocardiography of exposed embryos showed reduced cardiac function with both TCE and Benfluorex. Cardiac contraction was reduced by 29% and 23%, respectively at 10 ppb. The effects of TCE and Benfluorex on autocrine regulation of HNF4a, selected markers and cardiac function argue for a functional interaction of TCE and HNF4a. Further, the dose-sensitive shift between inhibition and induction of marker expression may explain the nonmonotonic-like dose response observed with TCE exposure in the heart.
- Selmin, O. (2017). Genistein reverses BRCA-1 CpG methylation in human breast cancer cells with activated AhR. Current Developments in Nutrition.
- Selmin, O. (2017). Prevention by food bioactives in relation to breast cancer subtype: Epigenetic mechanisms.. Epigenetics of Chemoprevention. Elsevier.
- Selmin, O. I. (2017). Mediterranean Diet: Prevention of Inflammatory Bowel Disease and Colorectal Cancer. Frontiers in Nutrition, 4, 59-65. doi:10.3389/fnut.2017.00059
- Makwana, O., Ahles, L., Lencinas, A., Selmin, O. I., & Runyan, R. B. (2013). Low-dose trichloroethylene alters cytochrome P450-2C subfamily expression in the developing chick heart. Cardiovascular Toxicology, 13(1), 77-84.More infoPMID: 22855351;PMCID: PMC3927724;Abstract: Trichloroethylene (TCE) is an organic solvent and common environmental contaminant. TCE exposure is associated with heart defects in humans and animal models. Primary metabolism of TCE in adult rodent models is by specific hepatic cytochrome P450 enzymes (Lash et al. in Environ Health Perspect 108:177-200, 2000). As association of TCE exposure with cardiac defects is in exposed embryos prior to normal liver development, we investigated metabolism of TCE in the early embryo. Developing chick embryos were dosed in ovo with environmentally relevant doses of TCE (8 and 800 ppb) and RNA was extracted from cardiac and extra-cardiac tissue (whole embryo without heart). Real-time PCR showed upregulation of CYP2H1 transcripts in response to TCE exposure in the heart. No detectable cytochrome expression was found in extra-cardiac tissue. As seen previously, the dose response was non-monotonic and 8 ppb elicited stronger upregulation than 800 ppb. Immunostaining for CYP2C subfamily expression confirmed protein expression and showed localization in both myocardium and endothelium. TCE exposure increased protein expression in both tissues. These data demonstrate that the earliest embryonic expression of phase I detoxification enzymes is in the developing heart. Expression of these CYPs is likely to be relevant to the susceptibility of the developing heart to environmental teratogens. © 2012 Springer Science+Business Media, LLC.
- Caldwell, P. T., Manziello, A., Howard, J., Palbykin, B., Runyan, R. B., & Selmin, O. (2010). Gene expression profiling in the fetal cardiac tissue after folate and low-dose trichloroethylene exposure. Birth Defects Research Part A - Clinical and Molecular Teratology, 88(2), 111-127.More infoPMID: 19813261;Abstract: BACKGROUND: Previous studies show gene expression alterations in rat embryo hearts and cell lines that correspond to the cardio-teratogenic effects of trichloroethylene (TCE) in animal models. One potential mechanism of TCE teratogenicity may be through altered regulation of calcium homeostatic genes with a corresponding inhibition of cardiac function. It has been suggested that TCE may interfere with the folic acid/methylation pathway in liver and kidney and alter gene regulation by epigenetic mechanisms. According to this hypothesis, folate supplementation in the maternal diet should counteract TCE effects on gene expression in the embryonic heart. APPROACH: To identify transcriptional targets altered in the embryonic heart after exposure to TCE, and possible protective effects of folate, we used DNA microarray technology to profile gene expression in embryonic mouse hearts with maternal TCE exposure and dietary changes in maternal folate. RESULTS: Exposure to low doses of TCE (10 ppb) caused extensive alterations in transcripts encoding proteins involved in transport, ion channel, transcription, differentiation, cytoskeleton, cell cycle, and apoptosis. Exogenous folate did not offset the effects of TCE exposure on normal gene expression, and both high and low levels of folate produced additional significant changes in gene expression. CONCLUSIONS: A mechanism by which TCE induces a folate deficiency does not explain altered gene expression patterns in the embryonic mouse heart. The data further suggest that use of folate supplementation, in the presence of this toxin, may be detrimental and not protective of the developing embryo © 2009 Wiley-Liss, Inc.
- Makwana, O., M., N., Ahles, L., Selmin, O., Granzier, H. L., & Runyan, R. B. (2010). Exposure to low-dose trichloroethylene alters shear stress gene expression and function in the developing chick heart. Cardiovascular Toxicology, 10(2), 100-107.More infoPMID: 20186580;PMCID: PMC3069695;Abstract: Trichloroethylene is an organic solvent used as an industrial degreasing agent. Due to its widespread use and volatile nature, TCE is a common environmental contaminant. Trichloroethylene exposure has been implicated in the etiology of heart defects in human populations and animal models. Recent data suggest misregulation of Ca2+ homeostasis in H9c2 cardiomyocyte cell line after TCE exposure. We hypothesized that misregulation of Ca2+ homeostasis alters myocyte function and leads to changes in embryonic blood flow. In turn, changes in cardiac flow are known to cause cardiac malformations. To investigate this hypothesis, we dosed developing chick embryos in ovo with environmentally relevant doses of TCE (8 and 800 ppb). RNA was isolated from control and treated embryos at specific times in development for real-time PCR analysis of blood flow markers. Effects were observed on Endothelin-1 (ET-1), Nitric Oxide Synthase-3 (NOS-3) and Krüppel-like Factor 2 (KLF2) expression relative to TCE exposure and consistent with reduced flow. Further, we measured function in the developing heart after TCE exposure by isolating cardiomyocytes and measuring half-width of contraction and sarcomere lengths. These functional data showed a significant increase in half-width of contraction after TCE exposure. These data suggest that perturbation of cardiac function contributes to the etiology of congenital heart defects in TCE-exposed embryos. © Springer Science+Business Media, LLC 2010.
- Petrick, J. S., Blachere, F. M., Selmin, O., & Lantz, R. C. (2009). Inorganic arsenic as a developmental toxicant: In utero exposure and alterations in the developing rat lungs. Molecular Nutrition and Food Research, 53(5), 583-591.More infoPMID: 19072884;PMCID: PMC2882184;Abstract: In the present study, we characterize the toxic effects of in utero arsenic exposure on the developing lung. We hypothesize that in utero exposure to inorganic arsenic through maternal drinking water causes altered gene and protein expression in the developing lung, indicative of downstream molecular and functional changes. From conception to embryonic day 18, we exposed pregnant Sprague-Dawley rats to 500 ppb arsenic (as arsenite) via the drinking water. Subtracted cDNA libraries comparing control to arsenic exposed embryonic lungs were generated. In addition, a broad Western blot analysis was performed to identify altered protein expression. A total of 59 genes and 34 proteins were identified as being altered. Pathway mapping and analysis showed that cell motility was the process most affected. The most likely affected pathway was alteration in integrin signaling through the b-catenin pathway, altering c-myc. The present study shows that arsenic induces alterations in the developing lung. These data may be useful in the elucidation of molecular targets and biomarkers of arsenic exposure during lung development and may aid in understanding the etiology of arsenic induced adult respiratory disease and lung cancers. © 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
- Caldwell, P. T., Thorne, P. A., Johnson, P. D., Boitano, S., Runyan, R. B., & Selmin, O. (2008). Trichloroethylene disrupts cardiac gene expression and calcium homeostasis in rat myocytes. Toxicological Sciences, 104(1), 135-143.More infoPMID: 18411232;PMCID: PMC4001797;Abstract: We have been investigating the molecular mechanisms by which trichloroethylene (TCE) might induce cardiac malformations in the embryonic heart. Previous results indicated that TCE disrupted expression of genes encoding proteins involved in regulation of intracellular Ca2+, [Ca2+]i, in cardiac cells, including ryanodine receptor isoform 2 (Ryr2), and sarcoendoplasmatic reticulum Ca2+ ATPase, Serca2a. These observations are important in light of the notion that altered cardiac contractility can produce morphological defects. The hypothesis tested in this study is that the TCE-induced changes in gene expression of Ca2+-associated proteins resulted in altered Ca2+ flux regulation. We used real-time PCR and digital imaging microscopy to characterize effects of various doses of TCE on gene expression and Ca2+ response to vasopressin (VP) in rat cardiac H9c2 myocytes. We observed a reduction in Serca2a and Ryr2 expression at 12 and 48 h after exposure to TCE. In addition, we found significant differences in Ca2+ response to VP in cells treated with TCE doses as low as 10 parts per billion. Taken all together, our data strongly indicate that exposure to TCE disrupts the ability of myocytes to regulate cellular Ca2+ fluxes. Perturbation of calcium signaling alters cardiac cell physiology and signal transduction and may hint to morphogenetic consequences in the context of heart development. These results point to a novel area of TCE biology and, if confirmed in vivo, may help to explain the apparent cardio-specific toxicity of TCE exposure in the rodent embryo. © The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved.
- Selmin, O. I., Thorne, P. A., Caldwell, P. T., & Taylor, M. R. (2008). Trichloroethylene and trichloroacetic acid regulate calcium signaling pathways in murine embryonal carcinoma cells P19. Cardiovascular Toxicology, 8(2), 47-56.More infoPMID: 18437584;Abstract: Trichloroethylene (TCE) and its metabolite trichloroacetic acid (TCA) are ubiquitous environmental contaminants which have been regarded as risk factors for congenital heart malformations. An increasing body of evidence from in vivo and in vitro studies supports the notion that exposure to TCE and TCA may interfere with normal embryonic heart development. The expression of several genes coding for factors implicated in the regulation of cardiac development has been shown to be modified by TCE or TCA, but the molecular mechanisms that mediate these effects are still obscure. In this study, we investigated the global changes in gene expression caused by exposure of P19 embryonal carcinoma cells to TCE and TCA, and whether or not TCE and/or TCA influence the expression levels of genes encoding for proteins that regulate calcium fluxes in cardiac cells. We report that TCE and TCA disrupt the expression of genes involved in processes important during embryonic development suggesting that exposure to environmentally significant concentrations of TCE may have deleterious effects on specific stages of cardiac differentiation. © 2008 Humana Press.
- Selmin, O., Thorne, P. A., Caldwell, P. T., Johnson, P. D., & Runyan, R. B. (2005). Effects of trichloroethylene and its metabolite trichloroacetic acid on the expression of vimentin in the rat H9c2 cell line. Cell Biology and Toxicology, 21(2), 83-95.More infoPMID: 16142583;Abstract: Trichloroethylene (TCE) and its metabolite trichloroacetic acid (TCAA) are environmental contaminants with specific toxicity for the embryonic heart. In an effort to identify the cellular pathways disrupted by TCE and TCAA during heart development, we investigated their effects on expression of vimentin, a marker of cardiac differentiation. Previous studies had shown that the level of vimentin transcript was inhibited in rat embryonic heart after maternal exposure to TCE via drinking water. In the same study, maternal exposure to TCAA produced the opposite effect, inducing an increased level of vimentin mRNA. In this study, we selected an in vitro system, the rat cardiac myoblast cell line H9c2, to further characterize the molecular mechanisms used by TCE and TCAA to disrupt normal heart development. In particular, we investigated the effects of both toxicants on vimentin, at both the RNA and protein levels, using dose-response and time course curves. Our experimental findings indicate that vimentin expression is affected by TCE and TCAA in H9c2 cells similarly as in vivo. The work is significant because it provides a suitable in vitro model for studies looking at toxicant effects on myocardiac cells, and it suggests that vimentin is a good marker of TCE exposure in the embryonic heart. © Springer 2005.
- Collier, J. M., Selmin, O., Johnson, P. D., & Runyan, R. B. (2003). Trichloroethylene effects on gene expression during cardiac development. Birth Defects Research Part A - Clinical and Molecular Teratology, 67(7), 488-495.More infoPMID: 14565619;Abstract: BACKGROUND: Halogenated hydrocarbon exposure is associated with changes in gene expression in adult and embryonic tissue. Our study was undertaken to identify differentially expressed mRNA transcripts in embryonic hearts from Sprague-Dawley rats exposed to trichloroethylene (TCE) or potential bio-transformation products dichloroethylene (DCE) and trichloroacetic acid (TCAA). METHODS: cDNA subtractive hybridization was used to selectively amplify expressed mRNA obtained from control or halogenated hydrocarbon exposed rat embryos. The doses used were 1100 and 110 ppm (8300 and 830 μM) TCE, 110 and 11 ppm (1100 and 110 μM) DCE, and 27.3 and 2.75 mg/ml (100 and 10 mM) TCAA. Control animals were given distilled drinking water throughout the period of experiments. RESULTS: Sequencing of over 100 clones derived from halogenated hydrocarbon exposed groups resulted in identification of numerous differentially regulated gene sequences. Up-regulated transcripts identified include genes associated with stress response (Hsp 70) and homeostasis (several ribosomal proteins). Down-regulated transcripts include extracellular matrix components (GPI-p137 and vimentin) and Ca2+ responsive proteins (Serca-2 Ca2+-ATPase and β-catenin). Two possible markers for fetal TCE exposure were identified: Serca-2 Ca2+-ATPase and GPI-p137, a GPI-linked protein of unknown function. Differential regulation of expression of both markers by TCE was confirmed by dot blot analysis and semi-quantitative RT-PCR with levels of TCE exposure between 100 and 250 ppb (0.76 and 1.9 μM) sufficient to decrease expression. CONCLUSIONS: Sequences down-regulated with TCE exposure appear to be those associated with cellular housekeeping, cell adhesion, and developmental processes, while TCE exposure up-regulates expression of numerous stress response and homeostatic genes. © 2003 Wiley-Liss, Inc.
- Helzlsouer, K. J., Selmin, O., Huang, H., Strickland, P. T., Hoffman, S., Alberg, A. J., Watson, M., Comstock, G. W., & Bell, D. (1998). Association between glutathione S-transferase M1, P1, and T1 genetic polymorphisms and development of breast cancer. Journal of the National Cancer Institute, 90(7), 512-518.More infoPMID: 9539246;Abstract: Background: Glutathione S-transferases (GSTs) are encoded by a superfamily of genes and play a role in the detoxification of potential carcinogens. In a nested case-control study, we investigated associations between genetic variability in specific GST genes (GSTM1, GSTT1, and GSTP1) and susceptibility to breast cancer. Methods: In 1989, a total of 32898 individuals donated blood samples to a research specimen bank established in Washington County, MD. Genotypes of blood specimen DNA were determined for 110 of 115 women with incident cases of breast cancer diagnosed during the period from 1990 through 1995 and up to 113 of 115 control subjects. Associations between specific genotypes and the development of breast cancer were examined by use of logistic regression to calculate odds ratios (ORs) and 95 % confidence intervals (CIs). Results: The GSTM1 homozygous null genotype was associated with an increased risk of developing breast cancer (OR = 2.10; 95 % CI = 1.22-3.64), principally due to an association with postmenopausal breast cancer (OR = 2.50; 95%CI = 1.34-4.65). For GSTP1, the data were suggestive of a trend of increasing risk with higher numbers of codon 105 valine alleles (compared with isoleucine alleles); a 1.97-fold increased risk of breast cancer (95% CI = 0.77-5.02) was associated with valine/valine homozygosity. The risk of breast cancer associated with the GSTT1 homozygous null genotype was 1.50 (95% CI = 0.76-2.95). The risk of breast cancer increased as the number of putative high-risk genotypes increased (P for trend
- Millikan, R. C., Pittman, G. S., Newman, B., Tse, C. J., Selmin, O., Rockhill, B., Savitz, D., Moorman, P. G., & Bell, D. A. (1998). Cigarette smoking, N-acetyltransferases 1 and 2, and breast cancer risk. Cancer Epidemiology Biomarkers and Prevention, 7(5), 371-378.More infoPMID: 9610785;Abstract: To examine the effects of smoking and N-acetylation genetics on breast cancer risk, we analyzed data from an ongoing, population-based, case- control study of invasive breast cancer in North Carolina. The study population consisted of 498 cases and 473 controls, with approximately equal numbers of African-American and white women, and women under the age of 50 and age 50 years or older. Among premenopausal women, there was no association between current smoking [odds ratio (OR), 0.9; 95% confidence interval (CI), 0.5-1.5] or past smoking (OR, 1.0; 95% CI, 0.6-1.6) and breast cancer risk. Among postmenopausal women, there was also no association with current smoking (OR, 1.2; 95% CI, 0.7-2.0); however, a small increase in risk was observed for past smoking (OR, 1.5; 95% CI, 1.0-2.4). For postmenopausal women who smoked in the past, ORs and 95% CIs were 3.4 (1.4-8.1) for smoking within the past 3 years, 3.0 (1.3-6.7) for smoking 4-9 years ago, and 0.6 (0.3-1.4) for smoking 10-19 years ago. Neither N-acetyltransferase 1 (NAT1) nor N-acetyltransferase 2 (NAT2) genotype alone was associated with increased breast cancer risk. There was little evidence for modification of smoking effects according to genotype, except among postmenopausal women. Among postmenopausal women, ORs for smoking within the past 3 years were greater for women with the NAT1*10 genotype (OR, 9.0; 95% CI, 1.9-41.8) than NAT1- non*10 (OR, 2.5; 95% CI, 0.9-7.2) and greater for NAT2-rapid genotype (OR, 7.4; 95% CI, 1.6-32.6) than NAT2-slow (OR, 2.8; 95% CI, 0.4-8.0). Future studies of NAT genotypes and breast cancer should investigate the effects of environmental tobacco smoke, diet, and other exposures.
- Lavigne, J. A., Helzlsouer, K. J., Huang, H., Strickland, P. T., Bell, D. A., Selmin, O., Watson, M. A., Hoffman, S., Comstock, G. W., & Yager, J. D. (1997). An association between the allele coding for a low activity variant of catechol-O-methyltransferase and the risk for breast cancer. Cancer Research, 57(24), 5493-5497.More infoPMID: 9407957;Abstract: Mounting evidence suggests that catechol metabolites of estradiol may contribute to the development of estrogen-induced cancers. O-Methylation, catalyzed by catechol-O-methyltransferase (COMT), inactivates catechol estrogens. COMT is polymorphic in the human population, with 25% of Caucasians being homozygous for a low activity allele of the enzyme (COMT(LL)). We hypothesized that low activity COMT may be a risk factor for human breast cancer and designed a PCR-based RFLP assay to determine COMT genotype in a cohort of 112 matched, nested case-control samples. In the total study population, the odds ratios for the association of breast cancer risk with COMT(HL) and COMT(LL) genotypes were 1.30 [confidence interval (CI), 0.66-2.58] and 1.45 (CI, 0.69-3.07), respectively. Postmenopausal COMT(LL) women had a greater than 2-fold increased risk of developing breast cancer [odds ratio (OR), 2.18; CI, 0.93-5.11]. The association of COMT(LL) with the development of postmenopausal breast cancer was stronger and statistically significant in those women with a body mass index >24.47 kg/m2 (OR, 3.58; CI, 1.07-11.98). When COMT(LL) was combined with either glutathione S-transferase (GST) M1 null or with GSTP1 Ile-105-Val/Val-105- Val (intermediate/low activity, respectively) genotypes, the risk for developing postmenopausal breast cancer was also significantly increased. Our findings suggest that the allele encoding low activity COMT may be an important contributor to the postmenopausal development of breast cancer in certain women.
- Selmin, O., Lucier, G. W., Clark, G. C., Tritscher, A. M., Heuvel, J. V., Gastel, J. A., Walker, N. J., Sutter, T. R., & Bell, D. A. (1996). Isolation and characterization of a novel gene induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver. Carcinogenesis, 17(12), 2609-2615.More infoPMID: 9006096;Abstract: The differential display technique was used to identify genes whose expression was regulated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Expression of a novel sequence was up-regulated in a dose-dependent fashion in liver of Sprague-Dawley male rats exposed to both chronic and acute treatment with TCDD, as measured by densitometry of Northern blot analyses (P < 0.01). A rapid amplification of cDNA ends (RACE) procedure was used to isolate a 1.8 kb cDNA from a rat liver cDNA preparation. This cloned cDNA, called 25-Dx, was sequenced and found to encode a peptide of 223 amino acids. In control rats, the 25-Dx gene was expressed at high levels in lung and liver. A hydrophobic domain of 14 residues followed by a proline-rich domain, both located in the N-terminal region, showed 71% homology with the transmembrane domain of the precursor for the interleukin-6 receptor and a conserved consensus sequence found in the cytokine/growth factor/prolactin receptor superfamily respectively.
- Selmin, O. (2018, April). Galangin is an epigenetic modulator of BRCA1 and induces estrogen receptor alpha in TNBC cells. AACR Conference Abstract #7597.
- Selmin, O. (2018, March). Flavones counteract epigenetic silencing of BRCA1 in breast cancer cells with activated AhR. CALS Poster Forum.
- Selmin, O. (2018, October). Arsenic-induced BRCA1CpG promoter methylation associates with downregulation of ERalpha and resistance to tamoxifen. 3rd annual University of Arizona Cancer Center Scientific Symposium and Retreat.