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Article ; Online: Anti-Inflammatory Mechanisms of Dietary Flavones: Tapping into Nature to Control Chronic Inflammation in Obesity and Cancer.

Kariagina, Anastasia / Doseff, Andrea I

International journal of molecular sciences

2022 Volume 23, Issue 24

Abstract: Flavones are natural phytochemicals broadly distributed in our diet. Their anti-inflammatory properties provide unique opportunities to control the innate immune system and inflammation. Here, we review the role of flavones in chronic inflammation with ... ...

Abstract	Flavones are natural phytochemicals broadly distributed in our diet. Their anti-inflammatory properties provide unique opportunities to control the innate immune system and inflammation. Here, we review the role of flavones in chronic inflammation with an emphasis on their impact on the molecular mechanisms underlying inflammatory diseases including obesity and cancer. Flavones can influence the innate immune cell repertoire restoring the immune landscape. Flavones impinge on NF-κB, STAT, COX-2, or NLRP3 inflammasome pathways reestablishing immune homeostasis. Devoid of adverse side effects, flavones could present alternative opportunities for the treatment and prevention of chronic inflammation that contributes to obesity and cancer.
Language	English
Publishing date	2022-12-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232415753
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Article ; Online: Benzophenone-3 alters expression of genes encoding vascularization and epithelial-mesenchymal transition functions during Trp53-null mammary tumorigenesis.

Morozova, Elena / Kariagina, Anastasia / Busch, Calista / Schwartz, Richard C

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2024 Volume 186, Page(s) 114540

Abstract: Benzophenone-3 (also referred to as oxybenzone) is a putative endocrine disrupting chemical and common ingredient in sunscreens and other personal care products. We previously showed that benzophenone-3 was promotional for epithelial tumorigenesis in ... ...

Abstract	Benzophenone-3 (also referred to as oxybenzone) is a putative endocrine disrupting chemical and common ingredient in sunscreens and other personal care products. We previously showed that benzophenone-3 was promotional for epithelial tumorigenesis in mice fed adult high-fat diet, while protective against the incidence of more aggressive spindle cell tumors in the same treatment group. In this study, we show that benzophenone-3 reduces epithelial to mesenchymal transition in the epithelial tumors of these mice. This reduction in epithelial to mesenchymal transition is associated with altered expression of several genes involved in regulation of angiogenesis and epithelial to mesenchymal transition. Among the genes altered in expression, Timp1 is of particular interest because benzophenone-3 suppressed both migration and Timp1 expression in a mammary tumor cell line that displays epithelial to mesenchymal transition characteristics. These alterations in gene expression plausibly stabilize the vasculature of epithelial carcinomas and contribute to benzophenone-3 promotion of epithelial tumors, while at the same time suppress epithelial to mesenchymal transition and suppress incidence of spindle cell tumors.
MeSH term(s)	Mice ; Animals ; Epithelial-Mesenchymal Transition ; Cell Transformation, Neoplastic ; Carcinogenesis/genetics ; Carcinoma ; Neovascularization, Pathologic ; Cell Line, Tumor ; Benzophenones
Chemical Substances	oxybenzone (95OOS7VE0Y) ; Benzophenones
Language	English
Publishing date	2024-02-20
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2024.114540
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Zs.A 529: Show issues

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Article ; Online: Genomic and metabolomic analysis of step-wise malignant transformation in human skin fibroblasts.

Kariagina, Anastasia / Lunt, Sophia Y / McCormick, J Justin

Carcinogenesis

2019 Volume 41, Issue 5, Page(s) 656–665

Abstract: Metabolic changes accompanying a step-wise malignant transformation was investigated using a syngeneic lineage of human fibroblasts. Cell immortalization was associated with minor alterations in metabolism. Consecutive loss of cell cycle inhibition in ... ...

Abstract	Metabolic changes accompanying a step-wise malignant transformation was investigated using a syngeneic lineage of human fibroblasts. Cell immortalization was associated with minor alterations in metabolism. Consecutive loss of cell cycle inhibition in immortalized cells resulted in increased levels of oxidative phosphorylation (OXPHOS). Overexpression of the H-Ras oncoprotein produced cells forming sarcomas in athymic mice. These transformed cells exhibited increased glucose consumption, glycolysis and a further increase in OXPHOS. Because of the markedly increased OXPHOS in transformed cells, the impact of a transaminase inhibitor, aminooxyacetic acid (AOA), which decreases glutamine influx to the tricarboxylic acid (TCA) cycle, was tested. Indeed, AOA significantly decreased proliferation of malignantly transformed fibroblasts and fibrosarcoma-derived cells in vitro and in vivo. AOA also decreased proliferation of cells susceptible to malignant transformation. Metabolomic studies in normal and transformed cells indicated that, in addition to the anticipated effect on the TCA cycle, AOA decreased production of nucleotides adenosine triphosphate (ATP) and uridine monophosphate. Exogenous nucleotides partially rescued decreased proliferation of the malignant cells treated with AOA. Our data indicate that AOA blocks several metabolic pathways essential for growth of malignant cells. Therefore, OXPHOS may provide important therapeutic targets for treatment of sarcoma.
MeSH term(s)	Aminooxyacetic Acid/pharmacology ; Animals ; Apoptosis ; Cell Proliferation ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Enzyme Inhibitors/pharmacology ; Female ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Fibrosarcoma/drug therapy ; Fibrosarcoma/genetics ; Fibrosarcoma/metabolism ; Fibrosarcoma/pathology ; Gene Expression Regulation, Neoplastic ; Genomics/methods ; Glycolysis ; Humans ; Metabolome/drug effects ; Mice ; Mice, Nude ; Oxidative Phosphorylation ; Skin/drug effects ; Skin/metabolism ; Skin/pathology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Enzyme Inhibitors ; Aminooxyacetic Acid (14I68GI3OQ)
Language	English
Publishing date	2019-07-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgz126
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Zs.A 1558: Show issues

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Article ; Online: Benzophenone-3 promotion of mammary tumorigenesis is diet-dependent.

Kariagina, Anastasia / Morozova, Elena / Hoshyar, Reyhane / Aupperlee, Mark D / Borin, Mitchell A / Haslam, Sandra Z / Schwartz, Richard C

Oncotarget

2020 Volume 11, Issue 48, Page(s) 4465–4478

Abstract: Benzophenone-3 is a putative endocrine disrupting chemical and common ingredient in sunscreens. The potential of endocrine disrupting chemicals to act as agonists or antagonists in critical hormonally regulated processes, such as mammary gland ... ...

Abstract	Benzophenone-3 is a putative endocrine disrupting chemical and common ingredient in sunscreens. The potential of endocrine disrupting chemicals to act as agonists or antagonists in critical hormonally regulated processes, such as mammary gland development and mammary tumorigenesis, demands evaluation of its potential in promoting breast cancer. This study identifies the effects of BP-3 on mammary tumorigenesis with high-fat diet during puberty versus adulthood in
Language	English
Publishing date	2020-12-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.27831
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Article: The Proliferative Response to p27 Down-Regulation in Estrogen Plus Progestin Hormonal Therapy is Lost in Breast Tumors.

Aupperlee, Mark D / Kariagina, Anastasia / Zaremba, Nicole / Basson, Marc D / Schwartz, Richard C / Haslam, Sandra Z

Translational oncology

2018 Volume 11, Issue 2, Page(s) 518–527

Abstract: Increased proliferation and breast cancer risk has been observed in postmenopausal women receiving estrogen (E) + progestin hormone replacement therapy (HRT). Progestin action is mediated through two progesterone receptor (PR) isoforms, PRA and PRB, with ...

Abstract	Increased proliferation and breast cancer risk has been observed in postmenopausal women receiving estrogen (E) + progestin hormone replacement therapy (HRT). Progestin action is mediated through two progesterone receptor (PR) isoforms, PRA and PRB, with unique transcriptional activity and function. The current study examines hormonal regulation of PR isoforms in the normal postmenopausal human breast and the mechanism by which progestins increase proliferation and breast cancer risk. Archival benign breast biopsies from postmenopausal and premenopausal women, and luminal breast tumor biopsies from postmenopausal women, were analyzed for regulation of PRA and PRB expression by E and E+medroxyprogesterone acetate (MPA). In the postmenopausal breast without HRT, PRA and PRB expression was decreased compared to the premenopausal breast. Both E (n = 12) and E+MPA (n = 13) HRT in the postmenopausal breast were associated with increased PRA and PRB expression, increased nuclear cyclin E expression, and decreased nuclear p27 expression compared to no HRT (n = 16). With E+MPA HRT, there was a further decrease in nuclear p27 and increased Receptor Activator of NF-kappa B Ligand (RANKL) expression compared to E-alone HRT. In luminal breast cancers, E+MPA HRT (n = 6) was also associated with decreased nuclear expression of the cell cycle inhibitor p27 compared to E HRT (n = 6), but was not associated with increased proliferation. These results suggest that p27 mediates progestin-induced proliferation in the normal human breast and that regulation of this proliferative response by E+MPA is lost in breast tumors.
Language	English
Publishing date	2018-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233 ; 1936-5233 ; 1944-7124
ISSN (online)	1936-5233
ISSN	1936-5233 ; 1944-7124
DOI	10.1016/j.tranon.2018.02.011
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Article ; Online: Progesterone stimulates proliferation and promotes cytoplasmic localization of the cell cycle inhibitor p27 in steroid receptor positive breast cancers.

Kariagina, Anastasia / Xie, Jianwei / Langohr, Ingeborg M / Opreanu, Razvan C / Basson, Marc D / Haslam, Sandra Z

Hormones & cancer

2013 Volume 4, Issue 6, Page(s) 381–390

Abstract: Progestins are reported to increase the risk of more aggressive estrogen receptor positive, progesterone receptor positive (ER+ PR+) breast cancers in postmenopausal women. Using an in vivo rat model of ER+ PR + mammary cancer, we show that tumors ... ...

Abstract	Progestins are reported to increase the risk of more aggressive estrogen receptor positive, progesterone receptor positive (ER+ PR+) breast cancers in postmenopausal women. Using an in vivo rat model of ER+ PR + mammary cancer, we show that tumors arising in the presence of estrogen and progesterone exhibit increased proliferation and decreased nuclear expression of the cell cycle inhibitor p27 compared with tumors growing in the presence of estrogen alone. In human T47D breast cancer cells, progestin increased proliferation and decreased nuclear p27 expression. The decrease of nuclear p27 protein was dependent on activation of Src and PI3K by progesterone receptor isoforms PRA or PRB. Importantly, increased proliferation and decreased nuclear p27 expression were observed in invasive breast carcinoma compared with carcinoma in situ. These results suggest that progesterone specifically regulates intracellular localization of p27 protein and proliferation. Therefore, progesterone-activated pathways can provide useful therapeutic targets for treatment of more aggressive ER+ PR+ breast cancers.
MeSH term(s)	Animals ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Cycle ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cytoplasm/metabolism ; Estrogens/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Molecular Targeted Therapy ; Progesterone/metabolism ; Protein Transport ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p21 ; Estrogens ; Progesterone (4G7DS2Q64Y)
Language	English
Publishing date	2013-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2543318-0
ISSN	1868-8500 ; 1868-8500
ISSN (online)	1868-8500
ISSN	1868-8500
DOI	10.1007/s12672-013-0159-5
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Article ; Online: Progesterone decreases levels of the adhesion protein E-cadherin and promotes invasiveness of steroid receptor positive breast cancers.

Kariagina, Anastasia / Xie, Jianwei / Langohr, Ingeborg M / Opreanu, Razvan C / Basson, Marc D / Haslam, Sandra Z

Hormones & cancer

2013 Volume 4, Issue 6, Page(s) 371–380

Abstract: Progestins are reported to increase the risk of invasive breast cancers in postmenopausal women receiving hormone therapy with estrogen plus progestin. We report here that estrogen and progesterone receptor positive (ER+PR+) rat mammary tumors arising in ...

Abstract	Progestins are reported to increase the risk of invasive breast cancers in postmenopausal women receiving hormone therapy with estrogen plus progestin. We report here that estrogen and progesterone receptor positive (ER+PR+) rat mammary tumors arising in the presence of estrogen and progesterone exhibit increased invasiveness and decreased expression of E-cadherin protein compared with tumors growing in the presence of estrogen alone. A similar decrease of E-cadherin expression was observed in human ER+PR+ invasive ductal carcinoma compared with ductal carcinoma in situ. In agreement with findings in the rat, estrogen plus progestin R5020 treatment decreased E-cadherin expression in vitro in T47D human breast cancer cells. Decrease of E-cadherin protein was mediated by progesterone receptor B (PRB) and dependent on the activation of the Wnt pathway. These results suggest that progesterone signaling via PRB contributes to tumor invasiveness and can provide an important therapeutic target for treatment of invasive ER+PR+ breast cancers.
MeSH term(s)	Animals ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cadherins/genetics ; Cadherins/metabolism ; Carcinoma, Ductal/metabolism ; Carcinoma, Ductal/pathology ; Cell Line, Tumor ; Estrogens/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Neoplasm Invasiveness ; Progesterone/metabolism ; Promegestone/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Progesterone/metabolism ; Wnt Signaling Pathway
Chemical Substances	Cadherins ; Estrogens ; Receptors, Progesterone ; progesterone receptor B ; Progesterone (4G7DS2Q64Y) ; Promegestone (9XE0V2SQYX)
Language	English
Publishing date	2013-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2543318-0
ISSN	1868-8500 ; 1868-8500
ISSN (online)	1868-8500
ISSN	1868-8500
DOI	10.1007/s12672-013-0158-6
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Article: Progesterone receptor isoform functions in normal breast development and breast cancer.

Kariagina, Anastasia / Aupperlee, Mark D / Haslam, Sandra Z

Critical reviews in eukaryotic gene expression

2008 Volume 18, Issue 1, Page(s) 11–33

Abstract: Progesterone acting through two isoforms of the progesterone receptor (PR), PRA and PRB, regulates proliferation and differentiation in the normal mammary gland in mouse, rat, and human. Progesterone and PR have also been implicated in the etiology and ... ...

Abstract	Progesterone acting through two isoforms of the progesterone receptor (PR), PRA and PRB, regulates proliferation and differentiation in the normal mammary gland in mouse, rat, and human. Progesterone and PR have also been implicated in the etiology and pathogenesis of human breast cancer. The focus of this review is recent advances in understanding the role of the PR isoform-specific functions in the normal breast and in breast cancer. Also discussed is information obtained from rodent studies and their relevance to our understanding of the role of progestins in breast cancer etiology.
MeSH term(s)	Animals ; Breast/growth & development ; Breast Neoplasms/metabolism ; Cyclin D1/genetics ; Cyclin D1/metabolism ; Cyclin-Dependent Kinase Inhibitor Proteins/genetics ; Cyclin-Dependent Kinase Inhibitor Proteins/metabolism ; Female ; Humans ; Mammary Glands, Animal/growth & development ; Mammary Glands, Human/growth & development ; Mice ; Phosphorylation ; Protein Isoforms/chemistry ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Rats ; Receptors, Progesterone/chemistry ; Receptors, Progesterone/genetics ; Receptors, Progesterone/metabolism ; Structure-Activity Relationship
Chemical Substances	Cyclin-Dependent Kinase Inhibitor Proteins ; Protein Isoforms ; Receptors, Progesterone ; Cyclin D1 (136601-57-5)
Language	English
Publishing date	2008-01-02
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1071345-1
ISSN	1045-4403
ISSN	1045-4403
DOI	10.1615/critreveukargeneexpr.v18.i1.20
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Zs.A 3226: Show issues

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Article ; Online: Amphiregulin mediates estrogen, progesterone, and EGFR signaling in the normal rat mammary gland and in hormone-dependent rat mammary cancers.

Kariagina, Anastasia / Xie, Jianwei / Leipprandt, Jeffrey R / Haslam, Sandra Z

Hormones & cancer

2010 Volume 1, Issue 5, Page(s) 229–244

Abstract: Both estrogen (E) and progesterone (P) are implicated in the etiology of human breast cancer. Defining their mechanisms of action, particularly in vivo, is relevant to the prevention and therapy of breast cancer. We investigated the molecular and ... ...

Abstract	Both estrogen (E) and progesterone (P) are implicated in the etiology of human breast cancer. Defining their mechanisms of action, particularly in vivo, is relevant to the prevention and therapy of breast cancer. We investigated the molecular and cellular mechanisms of E and/or P-induced in vivo proliferation, in the normal rat mammary gland and in hormone-dependent rat mammary cancers which share many characteristics with the normal human breast and hormone-dependent breast cancers. We show that E+P treatment induced significantly greater proliferation in both the normal gland and mammary cancers compared to E alone. In both the normal gland and tumors, E+P-induced proliferation was mediated through the increased production of amphiregulin (Areg), an epidermal growth factor receptor (EGFR) ligand, and the activation of intracellular signaling pathways (Erk, Akt, JNK) downstream of EGFR that regulate proliferation. In vitro experiments using rat primary mammary organoids or T47D breast cancer cells confirmed that Areg and the synthetic progestin, R5020, synergize to promote cell proliferation through EGFR signaling. Iressa, an EGFR inhibitor, effectively blocked this proliferation. These results indicate that mediators of cross talk between E, P, and EGFR pathways may be considered as relevant molecular targets for the therapy of hormone-dependent breast cancers, especially in premenopausal women.
MeSH term(s)	Amphiregulin ; Animals ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation ; EGF Family of Proteins ; ErbB Receptors/metabolism ; Estrogens/metabolism ; Female ; Gene Expression Regulation/physiology ; Glycoproteins/metabolism ; Humans ; Immunohistochemistry ; Intercellular Signaling Peptides and Proteins/metabolism ; Mammary Glands, Animal/metabolism ; Mammary Neoplasms, Experimental/metabolism ; Neoplasms, Hormone-Dependent/metabolism ; Progesterone/metabolism ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/physiology
Chemical Substances	AREG protein, human ; Amphiregulin ; Areg protein, rat ; EGF Family of Proteins ; Estrogens ; Glycoproteins ; Intercellular Signaling Peptides and Proteins ; Progesterone (4G7DS2Q64Y) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2010-11-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2543318-0
ISSN	1868-8500 ; 1868-8500
ISSN (online)	1868-8500
ISSN	1868-8500
DOI	10.1007/s12672-010-0048-0
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Article: Progesterone receptor isoforms and proliferation in the rat mammary gland during development.

Kariagina, Anastasia / Aupperlee, Mark D / Haslam, Sandra Z

Endocrinology

2007 Volume 148, Issue 6, Page(s) 2723–2736

Abstract: Progesterone (P), acting through progesterone receptor (PR) isoforms A and B, plays an important role in normal mammary gland development and is implicated in the etiology of breast cancer. Because of significant similarities between human and rat ... ...

Abstract	Progesterone (P), acting through progesterone receptor (PR) isoforms A and B, plays an important role in normal mammary gland development and is implicated in the etiology of breast cancer. Because of significant similarities between human and rat mammary gland development and hormonal responsiveness of mammary cancers, we investigated P action in the rat mammary gland. By immunohistochemical methods we determined PRA and PRB expression at puberty, sexual maturity, pregnancy, and lactation and after postlactational involution and their functional roles in the regulation of proliferation. PRA expression was restricted to luminal epithelial cells, whereas PRB was expressed in both luminal and myoepithelial cells, indicating a novel role of PRB in myoepithelial cell regulation. The majority of PRA-positive (PRA+) cells coexpressed PRB. In the pubertal and adult virgin mammary gland, PRA+PRB+ cells also expressed nuclear cyclin D1 but did not contain the proliferation marker bromodeoxyuridine. Based on a lack of phosphorylated retinoblastoma protein expression and the expression patterns of the cyclin-dependent kinase inhibitors p21 and p27 in these cells, we conclude that PRA+PRB+ cells appear to be cell cycle arrested and do not proliferate. PRA+ cells were decreased in the adult gland and during and after pregnancy. The percentage of PRB+ cells was relatively constant throughout development, and in a significant proportion of cells, only PRB was detected. During development, and especially during pregnancy, a high percentage of PRB+ cells were positive for bromodeoxyuridine. From this observation, we conclude that these cells proliferate and that P acting through PRB may directly stimulate proliferation.
MeSH term(s)	Animals ; Cell Proliferation ; Cyclin D1/metabolism ; Cyclin-Dependent Kinases/metabolism ; Female ; Gene Expression Regulation, Developmental ; Male ; Mammary Glands, Animal/growth & development ; Mammary Glands, Animal/metabolism ; Mice ; Organ Specificity ; Pregnancy ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Progesterone/genetics ; Receptors, Progesterone/metabolism ; Retinoblastoma Protein/metabolism ; Tissue Distribution
Chemical Substances	Protein Isoforms ; Receptors, Progesterone ; Retinoblastoma Protein ; progesterone receptor A ; progesterone receptor B ; Cyclin D1 (136601-57-5) ; Cyclin-Dependent Kinases (EC 2.7.11.22)
Language	English
Publishing date	2007-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2006-1493
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