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Article: Evaluation of Prevalence of PCOS and Associated Depression, Nutrition, and Family History: A Questionnaire-based Assessment.

Vishnubhotla, Deepa Switha / Tenali, Shouni Niveditha / Fernandez, Mini / Madireddi, Sujatha

Indian journal of endocrinology and metabolism

2022 Volume 26, Issue 4, Page(s) 341–347

Abstract: ... to understand the contribution of life style/nutrition to the risk of PCOS. Student's t test and Z proportion ... 56 m. Sizeable proportion reported irregular menstrual cycle (n=289;29.73%), that they get easily ...

Abstract	Context: Polycystic ovarian syndrome (PCOS) is a common condition affecting women in the prime of reproductive age. The symptoms include infertility, amenorrhea, hirsutism, obesity, and androgenic alopecia. It is a socially stigmatizing condition and is often associated with depression, poor mental health, and quality of life. Settings and design: We carried out a questionnaire based cross sectional study that assessed the prevalence of PCOS, collected information on the nutritional and life style related factors. A questionnaire was used to collect information with an intention to assess the prevalence of PCOS and to understand the contribution of life style/nutrition to the risk of PCOS. Student's t test and Z proportion test were used to assess significance and a 'p' value of ≤ 0.05 was considered significant. Results: A total of 972 females completed the questionnaire (mean age:24.37±8.37 years). Majority were from Telangana (n=823;84.67%) and students (690;70.98%). The mean weight was 60.58±13.03 kg and height was 1.78±2.56 m. Sizeable proportion reported irregular menstrual cycle (n=289;29.73%), that they get easily depressed: 283/972 (29.11%), low self-esteem:242/972 (24.90%), insomnia:223/972 (22.94%). A higher proportion of females were diabetic (8/243;3.29%Vs.10/706;1.42%;p=0.02) and non-vegetarian (69/243;28.40%Vs.119/706;16.86%;p=0.0002). No difference in the consumption of processed/fast food, carbonated drinks and lifestyle were noted. A significantly (p=0.0001) higher proportion of females had a positive family history (32/243;13.17%Vs.26/706;3.68%). Conclusion: Higher prevalence of PCOS was noted in young female population. Identifying at-risk individuals and imparting life style, nutrition-based modifications would be beneficial. Furthermore, regular counseling sessions might help tackle depression leading to a better overall physical and mental health.
Language	English
Publishing date	2022-09-20
Publishing country	India
Document type	Journal Article
ZDB-ID	2600211-5
ISSN	2230-9500 ; 2230-8210
ISSN (online)	2230-9500
ISSN	2230-8210
DOI	10.4103/ijem.ijem_467_21
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Article ; Online: CD8

Huseni, Mahrukh A / Wang, Lifen / Klementowicz, Joanna E / Yuen, Kobe / Breart, Beatrice / Orr, Christine / Liu, Li-Fen / Li, Yijin / Gupta, Vinita / Li, Congfen / Rishipathak, Deepali / Peng, Jing / Şenbabaoǧlu, Yasin / Modrusan, Zora / Keerthivasan, Shilpa / Madireddi, Shravan / Chen, Ying-Jiun / Fraser, Eleanor J / Leng, Ning /

Hamidi, Habib / Koeppen, Hartmut / Ziai, James / Hashimoto, Kenji / Fassò, Marcella / Williams, Patrick / McDermott, David F / Rosenberg, Jonathan E / Powles, Thomas / Emens, Leisha A / Hegde, Priti S / Mellman, Ira / Turley, Shannon J / Wilson, Mark S / Mariathasan, Sanjeev / Molinero, Luciana / Merchant, Mark / West, Nathaniel R

Cell reports. Medicine

2023 Volume 4, Issue 1, Page(s) 100878

Abstract: Although immune checkpoint inhibitors (ICIs) are established as effective cancer therapies, overcoming therapeutic resistance remains a critical challenge. Here we identify interleukin 6 (IL-6) as a correlate of poor response to atezolizumab (anti-PD-L1) ...

Abstract	Although immune checkpoint inhibitors (ICIs) are established as effective cancer therapies, overcoming therapeutic resistance remains a critical challenge. Here we identify interleukin 6 (IL-6) as a correlate of poor response to atezolizumab (anti-PD-L1) in large clinical trials of advanced kidney, breast, and bladder cancers. In pre-clinical models, combined blockade of PD-L1 and the IL-6 receptor (IL6R) causes synergistic regression of large established tumors and substantially improves anti-tumor CD8
MeSH term(s)	Animals ; Mice ; Antineoplastic Agents/therapeutic use ; B7-H1 Antigen/immunology ; B7-H1 Antigen/therapeutic use ; CD8-Positive T-Lymphocytes/metabolism ; Immunotherapy ; Interleukin-6/metabolism ; Neoplasms/immunology ; Neoplasms/therapy
Chemical Substances	Antineoplastic Agents ; atezolizumab (52CMI0WC3Y) ; B7-H1 Antigen ; Interleukin-6
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2022.100878
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Article ; Online: Regulatory T Cell-Mediated Suppression of Inflammation Induced by DR3 Signaling Is Dependent on Galectin-9.

Madireddi, Shravan / Eun, So-Young / Mehta, Amit K / Birta, Aruna / Zajonc, Dirk M / Niki, Toshiro / Hirashima, Mitsuomi / Podack, Eckhard R / Schreiber, Taylor H / Croft, Michael

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 199, Issue 8, Page(s) 2721–2728

Abstract: ... in murine models through augmenting the number and/or activity of regulatory T cells (Tregs). We recently ...

Abstract	Stimulation of several TNF receptor family proteins has been shown to dampen inflammatory disease in murine models through augmenting the number and/or activity of regulatory T cells (Tregs). We recently found that one molecule, 4-1BB, used binding to Galectin-9 to exert its immunosuppressive effects and drive expansion of CD8
MeSH term(s)	Animals ; Cell Proliferation ; Cells, Cultured ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Forkhead Transcription Factors/metabolism ; Galectins/genetics ; Galectins/metabolism ; Humans ; Immune Tolerance ; Inflammation/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Multiple Sclerosis/immunology ; Protein Binding ; Receptors, Tumor Necrosis Factor, Member 25/metabolism ; Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/immunology ; Tumor Necrosis Factor Receptor Superfamily, Member 9/metabolism
Chemical Substances	Forkhead Transcription Factors ; Foxp3 protein, mouse ; Galectins ; Receptors, Tumor Necrosis Factor, Member 25 ; Tnfrsf25 protein, mouse ; Tumor Necrosis Factor Receptor Superfamily, Member 9 ; galectin 9, mouse
Language	English
Publishing date	2017-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1700575
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Article ; Online: Homeostatic functions of monocytes and interstitial lung macrophages are regulated via collagen domain-binding receptor LAIR1.

Immunity

2021 Volume 54, Issue 7, Page(s) 1511–1526.e8

Abstract: Myeloid cells encounter stromal cells and their matrix determinants on a continual basis during their residence in any given organ. Here, we examined the impact of the collagen receptor LAIR1 on myeloid cell homeostasis and function. LAIR1 was highly ... ...

Abstract	Myeloid cells encounter stromal cells and their matrix determinants on a continual basis during their residence in any given organ. Here, we examined the impact of the collagen receptor LAIR1 on myeloid cell homeostasis and function. LAIR1 was highly expressed in the myeloid lineage and enriched in non-classical monocytes. Proteomic definition of the LAIR1 interactome identified stromal factor Colec12 as a high-affinity LAIR1 ligand. Proteomic profiling of LAIR1 signaling triggered by Collagen1 and Colec12 highlighted pathways associated with survival, proliferation, and differentiation. Lair1
MeSH term(s)	Animals ; Apoptosis/physiology ; Bone Marrow/metabolism ; Bone Marrow/pathology ; COS Cells ; Cell Differentiation/physiology ; Cell Line ; Cell Line, Tumor ; Cell Lineage/physiology ; Cell Proliferation/physiology ; Chlorocebus aethiops ; Female ; Homeostasis/physiology ; Humans ; Lung/metabolism ; Lung/pathology ; Macrophages, Alveolar/metabolism ; Macrophages, Alveolar/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monocytes/metabolism ; Monocytes/pathology ; Myeloid Cells/metabolism ; Myeloid Cells/pathology ; Neoplasm Metastasis/pathology ; Proteomics/methods ; Receptors, Immunologic/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptors, Immunologic ; leukocyte-associated immunoglobulin-like receptor 1
Language	English
Publishing date	2021-07-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2021.06.012
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Article ; Online: Intratumoral CD103+ CD8+ T cells predict response to PD-L1 blockade.

Banchereau, Romain / Chitre, Avantika S / Scherl, Alexis / Wu, Thomas D / Patil, Namrata S / de Almeida, Patricia / Kadel Iii, Edward E / Madireddi, Shravan / Au-Yeung, Amelia / Takahashi, Chikara / Chen, Ying-Jiun / Modrusan, Zora / McBride, Jacqueline / Nersesian, Rhea / El-Gabry, Ehab A / Robida, Mark D / Hung, Jeffrey C / Kowanetz, Marcin / Zou, Wei /

McCleland, Mark / Caplazi, Patrick / Eshgi, Shadi Toghi / Koeppen, Hartmut / Hegde, Priti S / Mellman, Ira / Mathews, W Rodney / Powles, Thomas / Mariathasan, Sanjeev / Grogan, Jane / O'Gorman, William E

Journal for immunotherapy of cancer

2021 Volume 9, Issue 4

Abstract: Background: CD8+ tissue-resident memory T (T: Methods: Here, we test this by combining high ... Conclusions: Our analyses indeed demonstrate that the presence of CD103+ CD8+ T ...

Abstract	Background: CD8+ tissue-resident memory T (T Methods: Here, we test this by combining high-dimensional single-cell modalities with bulk tumor transcriptomics from 1868 patients enrolled in lung and bladder cancer clinical trials of atezolizumab (anti-programmed cell death ligand 1 (PD-L1)). Results: ITGAE Conclusions: Our analyses indeed demonstrate that the presence of CD103+ CD8+ T
MeSH term(s)	Antibodies, Monoclonal, Humanized/adverse effects ; Antibodies, Monoclonal, Humanized/therapeutic use ; Antigens, CD/genetics ; B7-H1 Antigen/antagonists & inhibitors ; B7-H1 Antigen/immunology ; Biomarkers, Tumor/genetics ; CD8-Positive T-Lymphocytes/immunology ; Clinical Trials, Phase II as Topic ; Clinical Trials, Phase III as Topic ; Databases, Genetic ; Gene Expression Profiling ; Humans ; Immune Checkpoint Inhibitors/adverse effects ; Immune Checkpoint Inhibitors/therapeutic use ; Integrin alpha Chains/genetics ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/immunology ; Lymphocytes, Tumor-Infiltrating/immunology ; Phenotype ; Randomized Controlled Trials as Topic ; Time Factors ; Treatment Outcome ; Tumor Microenvironment ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/immunology
Chemical Substances	Antibodies, Monoclonal, Humanized ; Antigens, CD ; B7-H1 Antigen ; Biomarkers, Tumor ; CD274 protein, human ; Immune Checkpoint Inhibitors ; Integrin alpha Chains ; alpha E integrins ; atezolizumab (52CMI0WC3Y)
Language	English
Publishing date	2021-04-07
Publishing country	England
Document type	Journal Article
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2020-002231
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Article ; Online: Galectin-9 controls the therapeutic activity of 4-1BB-targeting antibodies.

Madireddi, Shravan / Eun, So-Young / Lee, Seung-Woo / Nemčovičová, Ivana / Mehta, Amit Kumar / Zajonc, Dirk M / Nishi, Nozomu / Niki, Toshiro / Hirashima, Mitsuomi / Croft, Michael

The Journal of experimental medicine

2014 Volume 211, Issue 7, Page(s) 1433–1448

Abstract: ... promote regulatory T cells that inhibit autoimmune disease. We found that the action of agonist anti-4-1BB ... 1BB, and Gal-9 facilitated 4-1BB aggregation, signaling, and functional activity in T cells, dendritic ...

Abstract	Biologics to TNF family receptors are prime candidates for therapy of immune disease. Whereas recent studies have highlighted a requirement for Fcγ receptors in enabling the activity of CD40, TRAILR, and GITR when engaged by antibodies, other TNFR molecules may be controlled by additional mechanisms. Antibodies to 4-1BB (CD137) are currently in clinical trials and can both augment immunity in cancer and promote regulatory T cells that inhibit autoimmune disease. We found that the action of agonist anti-4-1BB in suppressing autoimmune and allergic inflammation was completely dependent on Galectin-9 (Gal-9). Gal-9 directly bound to 4-1BB, in a site distinct from the binding site of antibodies and the natural ligand of 4-1BB, and Gal-9 facilitated 4-1BB aggregation, signaling, and functional activity in T cells, dendritic cells, and natural killer cells. Conservation of the Gal-9 interaction in humans has important implications for effective clinical targeting of 4-1BB and possibly other TNFR superfamily molecules.
MeSH term(s)	Animals ; Antibodies/immunology ; Antibodies/pharmacology ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Galectins/genetics ; Galectins/immunology ; Humans ; Hypersensitivity/drug therapy ; Hypersensitivity/genetics ; Hypersensitivity/immunology ; Mice ; Mice, Knockout ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/immunology ; T-Lymphocytes, Regulatory/immunology ; Tumor Necrosis Factor Receptor Superfamily, Member 9/antagonists & inhibitors ; Tumor Necrosis Factor Receptor Superfamily, Member 9/genetics ; Tumor Necrosis Factor Receptor Superfamily, Member 9/immunology
Chemical Substances	Antibodies ; Galectins ; LGALS9 protein, human ; Tumor Necrosis Factor Receptor Superfamily, Member 9 ; galectin 9, mouse
Language	English
Publishing date	2014-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20132687
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Article: Regulation of mda-7 gene expression during human melanoma differentiation.

Madireddi, M T / Dent, P / Fisher, P B

Oncogene

2000 Volume 19, Issue 10, Page(s) 1362–1368

Abstract: Induction of irreversible growth arrest and terminal differentiation in human melanoma cells following treatment with recombinant human fibroblast interferon (IFN-beta) and mezerein (MEZ) results in elevated expression of a specific melanoma ... ...

Abstract	Induction of irreversible growth arrest and terminal differentiation in human melanoma cells following treatment with recombinant human fibroblast interferon (IFN-beta) and mezerein (MEZ) results in elevated expression of a specific melanoma differentiation associated gene, mda-7. Experiments were conducted to define the mechanism involved in the regulation of mda-7 expression in differentiating human melanoma cells. The mda-7 gene is actively transcribed in uninduced HO-1 human melanoma cells and the rate of transcription of mda-7 is not significantly enhanced by treatment with IFN-beta, MEZ or IFN-beta+MEZ. The high basal activity of the mda-7 promoter in uninduced melanoma cells and the absence of enhancing effect upon treatment with differentiation inducers is corroborated by transfection studies using the promoter region of mda-7 linked to a luciferase reporter gene containing the SV40 polyadenylation signal sequence. RT - PCR analysis detects the presence of low levels of mda-7 transcripts in uninduced and concomitant increases in differentiation inducer treated HO-1 cells. However, steady-state mda-7 mRNA is detected only in IFN-beta+MEZ and to a lesser degree in MEZ treated cells. We show that induction of terminal differentiation of HO-1 cells with IFN-beta+MEZ dramatically increases the half-life of mda-7 mRNA while treatment with cycloheximide results in detectable mda-7 mRNA in control and inducer treated cells. These observations confirm constitutive activity of the mda-7 promoter in HO-1 cells irrespective of differentiation status suggesting posttranscriptional processes as important determinants of mda-7 expression during terminal differentiation. The 3' UTR region of mda-7 contains AU-rich elements (ARE) that contribute to rapid mda-7 mRNA turnover during proliferation and reversible differentiation, a process controlled by a labile protein factor(s). Substitution of the SV40 polyadenylation signal sequence in the luciferase reporter plasmid with the mda-7-ARE-3'-UTR renders the Luciferase message unstable when expressed in proliferating and reversibly differentiated melanoma cells. In contrast, the luciferase message is stabilized when the mda-7-ARE-3'-UTR construct is expressed in terminally differentiated HO-1 cells. These results provide compelling evidence that mda-7 expression during terminal differentiation in human melanoma cells is regulated predominantly at a posttranscriptional level.
MeSH term(s)	3' Untranslated Regions ; Base Sequence ; Cell Differentiation ; Cloning, Molecular ; Cycloheximide/pharmacology ; Dactinomycin/pharmacology ; Diterpenes ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Growth Substances/biosynthesis ; Growth Substances/genetics ; Humans ; Interferon-beta/pharmacology ; Interleukins ; Melanoma/genetics ; Melanoma/pathology ; Molecular Sequence Data ; Promoter Regions, Genetic ; RNA Processing, Post-Transcriptional ; RNA Stability/drug effects ; RNA, Messenger/metabolism ; Terpenes/pharmacology
Chemical Substances	3' Untranslated Regions ; Diterpenes ; Growth Substances ; Interleukins ; RNA, Messenger ; Terpenes ; interleukin-24 ; Dactinomycin (1CC1JFE158) ; mezerein (34807-41-5) ; Interferon-beta (77238-31-4) ; Cycloheximide (98600C0908)
Language	English
Publishing date	2000-03-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/sj.onc.1203424
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Article: AP-1 and C/EBP transcription factors contribute to mda-7 gene promoter activity during human melanoma differentiation.

Madireddi, M T / Dent, P / Fisher, P B

Journal of cellular physiology

2000 Volume 185, Issue 1, Page(s) 36–46

Abstract: Treatment of human melanoma cells with a combination of recombinant fibroblast interferon (IFN-beta) and the protein kinase C (PKC) activator mezerein (MEZ) causes a rapid and irreversible suppression in growth and terminal cell differentiation. Temporal ...

Abstract	Treatment of human melanoma cells with a combination of recombinant fibroblast interferon (IFN-beta) and the protein kinase C (PKC) activator mezerein (MEZ) causes a rapid and irreversible suppression in growth and terminal cell differentiation. Temporal subtraction hybridization combined with random clone selection, reverse Northern hybridization, high throughput microchip cDNA array screening, and serial cDNA library arrays permit the identification and cloning of genes that are differentially expressed during proliferative arrest and terminal differentiation in human melanoma cells. A specific melanoma differentiation associated (mda) gene, mda-7, exhibits reduced expression as a function of melanoma progression from melanocyte to metastatic melanoma. In contrast, treatment of metastatic melanoma cells with IFN-beta + MEZ results in expression of mda-7 mRNA and protein. To evaluate the mechanism underlying the differential expression of mda-7 as a function of melanoma progression and induction of growth arrest and differentiation in human melanoma cells the promoter region of this gene has been isolated from a human placental genomic library and characterized. Sequence analysis by GCG identifies multiple recognition sites for the AP-1 and C/EBP transcription factors. Employing a heterologous mda-7 luciferase gene reporter system, we demonstrate that ectopic expression of either AP-1/cJun or C/EBP can significantly enhance expression of the mda-7 promoter in melanoma cells. In contrast, a dominant negative mutant of cJun, TAM67, is devoid of promoter-enhancing ability. Western blot analyses reveals that cJun and the C/EBP family member C/EBP-beta are physiologically relevant transcription factors whose expression corresponds with mda-7 mRNA expression. Electrophoretic mobility shift assays (EMSA) performed using nuclear protein extracts from terminally differentiated human melanoma cells document binding to regions of the mda-7 promoter that correspond to consensus binding sites for AP-1 and C/EBP. These results provide further mechanistic insights into the regulation of the mda-7 gene during induction of terminal cell differentiation in human melanoma cells.
MeSH term(s)	Base Sequence ; CCAAT-Enhancer-Binding Proteins ; Cell Differentiation/genetics ; Cloning, Molecular ; DNA, Complementary/genetics ; DNA, Complementary/isolation & purification ; DNA-Binding Proteins/genetics ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Growth Substances/genetics ; Humans ; Interleukins ; Melanoma/genetics ; Melanoma/pathology ; Molecular Sequence Data ; Nuclear Proteins/genetics ; Promoter Regions, Genetic/genetics ; Transcription Factor AP-1/genetics ; Tumor Cells, Cultured
Chemical Substances	CCAAT-Enhancer-Binding Proteins ; DNA, Complementary ; DNA-Binding Proteins ; Growth Substances ; Interleukins ; Nuclear Proteins ; Transcription Factor AP-1 ; interleukin-24
Language	English
Publishing date	2000-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/1097-4652(200010)185:1<36::AID-JCP3>3.0.CO;2-V
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Article ; Online: Tetravalent biepitopic targeting enables intrinsic antibody agonism of tumor necrosis factor receptor superfamily members.

mAbs

2019 Volume 11, Issue 6, Page(s) 996–1011

Abstract: Agonism of members of the tumor necrosis factor receptor superfamily (TNFRSF) with monoclonal antibodies is of high therapeutic interest due to their role in immune regulation and cell proliferation. A major hurdle for pharmacologic activation of this ... ...

Abstract	Agonism of members of the tumor necrosis factor receptor superfamily (TNFRSF) with monoclonal antibodies is of high therapeutic interest due to their role in immune regulation and cell proliferation. A major hurdle for pharmacologic activation of this receptor class is the requirement for high-order clustering, a mechanism that imposes a reliance
MeSH term(s)	Animals ; Antibodies, Monoclonal/immunology ; CD28 Antigens/immunology ; CHO Cells ; Cricetulus ; Humans ; Immunologic Capping ; Jurkat Cells ; Mice ; Mice, SCID ; Mice, Transgenic ; OX40 Ligand/agonists ; OX40 Ligand/immunology ; Receptors, Fc/immunology ; Receptors, TNF-Related Apoptosis-Inducing Ligand/agonists ; Receptors, TNF-Related Apoptosis-Inducing Ligand/immunology ; Signal Transduction/immunology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology
Chemical Substances	Antibodies, Monoclonal ; CD28 Antigens ; OX40 Ligand ; Receptors, Fc ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; TNFRSF10B protein, human ; TNFSF4 protein, human
Language	English
Publishing date	2019-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Video-Audio Media
ISSN	1942-0870
ISSN (online)	1942-0870
DOI	10.1080/19420862.2019.1625662
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Article ; Online: Targeting Calcium Signaling Induces Epigenetic Reactivation of Tumor Suppressor Genes in Cancer.

Cancer research

2016 Volume 76, Issue 6, Page(s) 1494–1505

Abstract: Targeting epigenetic pathways is a promising approach for cancer therapy. Here, we report on the unexpected finding that targeting calcium signaling can reverse epigenetic silencing of tumor suppressor genes (TSG). In a screen for drugs that reactivate ... ...

Abstract	Targeting epigenetic pathways is a promising approach for cancer therapy. Here, we report on the unexpected finding that targeting calcium signaling can reverse epigenetic silencing of tumor suppressor genes (TSG). In a screen for drugs that reactivate silenced gene expression in colon cancer cells, we found three classical epigenetic targeted drugs (DNA methylation and histone deacetylase inhibitors) and 11 other drugs that induced methylated and silenced CpG island promoters driving a reporter gene (GFP) as well as endogenous TSGs in multiple cancer cell lines. These newly identified drugs, most prominently cardiac glycosides, did not change DNA methylation locally or histone modifications globally. Instead, all 11 drugs altered calcium signaling and triggered calcium-calmodulin kinase (CamK) activity, leading to MeCP2 nuclear exclusion. Blocking CamK activity abolished gene reactivation and cancer cell killing by these drugs, showing that triggering calcium fluxes is an essential component of their epigenetic mechanism of action. Our data identify calcium signaling as a new pathway that can be targeted to reactivate TSGs in cancer.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Calcium/metabolism ; Calcium Signaling/drug effects ; Calcium Signaling/genetics ; Cell Line ; Cell Line, Tumor ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/genetics ; CpG Islands/drug effects ; CpG Islands/genetics ; DNA Methylation/drug effects ; DNA Methylation/genetics ; Epigenesis, Genetic/drug effects ; Epigenesis, Genetic/genetics ; Epigenomics/methods ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/genetics ; Gene Silencing/drug effects ; Genes, Tumor Suppressor/drug effects ; HCT116 Cells ; HEK293 Cells ; HL-60 Cells ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; K562 Cells ; Nuclear Proteins/genetics ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/genetics ; Signal Transduction/drug effects ; Signal Transduction/genetics
Chemical Substances	Antineoplastic Agents ; Histone Deacetylase Inhibitors ; Nuclear Proteins ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2016-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-14-2391
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