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Article ; Online: MST4: A Potential Oncogene and Therapeutic Target in Breast Cancer.

Arora, Ritu / Kim, Jin-Hwan / Getu, Ayechew A / Angajala, Anusha / Chen, Yih-Lin / Wang, Bin / Kahn, Andrea G / Chen, Hong / Reshi, Latif / Lu, Jianrong / Zhang, Wenling / Zhou, Ming / Tan, Ming

Cells

2022 Volume 11, Issue 24

Abstract: The mammalian STE 20-like protein kinase 4 (MST4) gene is highly expressed in several cancer types, but little is known about the role of MST4 in breast cancer, and the function of MST4 during epithelial-mesenchymal transition (EMT) has not been fully ... ...

Abstract	The mammalian STE 20-like protein kinase 4 (MST4) gene is highly expressed in several cancer types, but little is known about the role of MST4 in breast cancer, and the function of MST4 during epithelial-mesenchymal transition (EMT) has not been fully elucidated. Here we report that overexpression of MST4 in breast cancer results in enhanced cell growth, migration, and invasion, whereas inhibition of MST4 expression significantly attenuates these properties. Further study shows that MST4 promotes EMT by activating Akt and its downstream signaling molecules such as E-cadherin/N-cadherin, Snail, and Slug. MST4 also activates AKT and its downstream pro-survival pathway. Furthermore, by analyzing breast cancer patient tissue microarray and silicon datasets, we found that MST4 expression is much higher in breast tumor tissue compared to normal tissue, and significantly correlates with cancer stage, lymph node metastasis and a poor overall survival rate (
MeSH term(s)	Female ; Humans ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Epithelial-Mesenchymal Transition/genetics ; Lymphatic Metastasis ; Oncogenes ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Protein Serine-Threonine Kinases/genetics
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; STK26 protein, human (EC 2.7.1.-) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-12-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11244057
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: MicroRNAs within the Basal-like signature of Quadruple Negative Breast Cancer impact overall survival in African Americans.

Angajala, Anusha / Raymond, Hughley / Muhammad, Aliyu / Uddin Ahmed, Md Shakir / Haleema, Saadia / Haque, Monira / Wang, Honghe / Campbell, Moray / Martini, Rachel / Karanam, Balasubramanian / Kahn, Andrea G / Bedi, Deepa / Davis, Melissa / Tan, Ming / Dean-Colomb, Windy / Yates, Clayton

Scientific reports

2022 Volume 12, Issue 1, Page(s) 22178

Abstract: We previously found that QNBC tumors are more frequent in African Americans compared to TNBC tumors. To characterize this subtype further, we sought to determine the miRNA-mRNA profile in QNBC patients based on race. Both miRNA and mRNA expression data ... ...

Abstract	We previously found that QNBC tumors are more frequent in African Americans compared to TNBC tumors. To characterize this subtype further, we sought to determine the miRNA-mRNA profile in QNBC patients based on race. Both miRNA and mRNA expression data were analyzed from TCGA and validated using datasets from the METABRIC, TCGA proteomic, and survival analysis by KMPLOT. miRNA-mRNAs which include FOXA1 and MYC (mir-17/20a targets); GATA3 and CCNG2 (mir-135b targets); CDKN2A, CDK6, and B7-H3 (mir-29c targets); and RUNX3, KLF5, IL1-β, and CTNNB1 (mir-375 targets) were correlated with basal-like and immune subtypes in QNBC patients and associated with a worse survival. Thus, QNBC tumors have an altered gene signature implicated in racial disparity and poor survival.
MeSH term(s)	Humans ; Female ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology ; Black or African American/genetics ; Proteomics ; RNA, Messenger ; Gene Expression Regulation, Neoplastic
Chemical Substances	MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2022-12-22
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-26000-9
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Article ; Online: Primary saturation of α, β-unsaturated carbonyl containing fatty acids does not abolish electrophilicity.

Snyder, Nathaniel W / O'Brien, James / Singh, Bhupinder / Buchan, Gregory / Arroyo, Alejandro D / Liu, Xiaojing / Bostwick, Anna / Varner, Erika L / Angajala, Anusha / Sobol, Robert W / Blair, Ian A / Mesaros, Clementina / Wendell, Stacy G

Chemico-biological interactions

2021 Volume 350, Page(s) 109689

Abstract: Metabolism of polyunsaturated fatty acids results in the formation of hydroxylated fatty acids that can be further oxidized by dehydrogenases, often resulting in the formation of electrophilic, α,β-unsaturated ketone containing fatty acids. As ... ...

Abstract	Metabolism of polyunsaturated fatty acids results in the formation of hydroxylated fatty acids that can be further oxidized by dehydrogenases, often resulting in the formation of electrophilic, α,β-unsaturated ketone containing fatty acids. As electrophiles are associated with redox signaling, we sought to investigate the metabolism of the oxo-fatty acid products in relation to their double bond architecture. Using an untargeted liquid chromatography mass spectrometry approach, we identified mono- and di-saturated products of the arachidonic acid-derived 11-oxoeicosatetraenoic acid (11-oxoETE) and mono-saturated metabolites of 15-oxoETE and docosahexaenoic acid-derived 17-oxodocosahexaenoinc acid (17-oxoDHA) in both human A549 lung carcinoma and umbilical vein endothelial cells. Notably, mono-saturated oxo-fatty acids maintained their electrophilicity as determined by nucleophilic conjugation to glutathione while a second saturation of 11-oxoETE resulted in a loss of electrophilicity. These results would suggest that prostaglandin reductase 1 (PTGR1), known only for its reduction of the α,β-unsaturated double bond, was not responsible for the saturation of oxo-fatty acids at alternative double bonds. Surprisingly, knockdown of PTGR1 expression by shRNA confirmed its participation in the formation of 15-oxoETE and 17-oxoDHA mono-saturated metabolites. Furthermore, overexpression of PTGR1 in A549 cells increased the rate and total amount of oxo-fatty acid saturation. These findings will further facilitate the study of electrophilic fatty acid metabolism and signaling in the context of inflammatory diseases and cancer where they have been shown to have anti-inflammatory and anti-proliferative signaling properties.
MeSH term(s)	A549 Cells ; Alcohol Oxidoreductases/antagonists & inhibitors ; Alcohol Oxidoreductases/genetics ; Alcohol Oxidoreductases/metabolism ; Arachidonic Acids/chemistry ; Arachidonic Acids/metabolism ; Chromatography, Liquid ; Docosahexaenoic Acids/chemistry ; Docosahexaenoic Acids/metabolism ; Electrochemistry ; Fatty Acids, Monounsaturated/chemistry ; Fatty Acids, Monounsaturated/metabolism ; Fatty Acids, Unsaturated/chemistry ; Fatty Acids, Unsaturated/metabolism ; Gene Knockdown Techniques ; Human Umbilical Vein Endothelial Cells ; Humans ; Oxidation-Reduction ; Signal Transduction ; Tandem Mass Spectrometry ; Up-Regulation
Chemical Substances	11-oxoeicosatetraenoic acid ; 15-oxo-5,8,11,13-eicosatetraenoic acid ; Arachidonic Acids ; Fatty Acids, Monounsaturated ; Fatty Acids, Unsaturated ; Docosahexaenoic Acids (25167-62-8) ; Alcohol Oxidoreductases (EC 1.1.-) ; leukotriene B4 12-hydroxydehydrogenase (EC 1.1.1.-)
Language	English
Publishing date	2021-10-08
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	218799-1
ISSN	1872-7786 ; 0009-2797
ISSN (online)	1872-7786
ISSN	0009-2797
DOI	10.1016/j.cbi.2021.109689
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Article ; Online: NAD

Li, Jianfeng / M Saville, Kate / Ibrahim, Md / Zeng, Xuemei / McClellan, Steve / Angajala, Anusha / Beiser, Alison / Andrews, Joel F / Sun, Mai / Koczor, Christopher A / Clark, Jennifer / Hayat, Faisal / Makarov, Mikhail V / Wilk, Anna / Yates, Nathan A / Migaud, Marie E / Sobol, Robert W

NAR cancer

2021 Volume 3, Issue 4, Page(s) zcab044

Abstract: Elevated expression of the DNA damage response proteins PARP1 and poly(ADP-ribose) glycohydrolase (PARG) in glioma stem cells (GSCs) suggests that glioma may be a unique target for PARG inhibitors (PARGi). While PARGi-induced cell death is achieved when ... ...

Abstract	Elevated expression of the DNA damage response proteins PARP1 and poly(ADP-ribose) glycohydrolase (PARG) in glioma stem cells (GSCs) suggests that glioma may be a unique target for PARG inhibitors (PARGi). While PARGi-induced cell death is achieved when combined with ionizing radiation, as a single agent PARG inhibitors appear to be mostly cytostatic. Supplementation with the NAD
Language	English
Publishing date	2021-11-17
Publishing country	England
Document type	Journal Article
ISSN	2632-8674
ISSN (online)	2632-8674
DOI	10.1093/narcan/zcab044
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Article: Diverse Roles of Mitochondria in Immune Responses: Novel Insights Into Immuno-Metabolism.

Angajala, Anusha / Lim, Sangbin / Phillips, Joshua B / Kim, Jin-Hwan / Yates, Clayton / You, Zongbing / Tan, Ming

Frontiers in immunology

2018 Volume 9, Page(s) 1605

Abstract: Lack of immune system cells or impairment in differentiation of immune cells is the basis for many chronic diseases. Metabolic changes could be the root cause for this immune cell impairment. These changes could be a result of altered transcription, ... ...

Abstract	Lack of immune system cells or impairment in differentiation of immune cells is the basis for many chronic diseases. Metabolic changes could be the root cause for this immune cell impairment. These changes could be a result of altered transcription, cytokine production from surrounding cells, and changes in metabolic pathways. Immunity and mitochondria are interlinked with each other. An important feature of mitochondria is it can regulate activation, differentiation, and survival of immune cells. In addition, it can also release signals such as mitochondrial DNA (mtDNA) and mitochondrial ROS (mtROS) to regulate transcription of immune cells. From current literature, we found that mitochondria can regulate immunity in different ways.
Language	English
Publishing date	2018-07-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.01605
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Article: Quadruple Negative Breast Cancers (QNBC) Demonstrate Subtype Consistency among Primary and Recurrent or Metastatic Breast Cancer.

Angajala, Anusha / Mothershed, Essynce / Davis, Melissa B / Tripathi, Shweta / He, Qinghua / Bedi, Deepa / Dean-Colomb, Windy / Yates, Clayton

Translational oncology

2018 Volume 12, Issue 3, Page(s) 493–501

Abstract: Purpose: Despite the availability of current standards of care treatments for triple negative breast cancer (TNBC), many patients still die from this disease. Quadruple negative tumors, which are TNBC tumors that lack androgen receptor (AR), represent a ...

Abstract	Purpose: Despite the availability of current standards of care treatments for triple negative breast cancer (TNBC), many patients still die from this disease. Quadruple negative tumors, which are TNBC tumors that lack androgen receptor (AR), represent a more aggressive subtype of TNBC; however, the molecular features are not well understood. Methods: Immunohistochemistry of estrogen receptor (ER), progesterone receptor (PR), HER2, and AR was determined in 244 primary and 630 recurrent/metastatic site biopsies. Expression was correlated with a panel of 25 cancer-related genes and proteins by IHC and in situ hybridization (ISH). Results: We observed that 80.2% (65 of 81) of primary TNBC tumors and 75.7% (159 of 210) of recurrent/metastatic TNBC tumors are QNBC. Bivariate fit analysis demonstrated that QNBC (n = 224) significantly (P < .03) correlated with younger aged patients at initial biopsy compared to AR positive TNBC patients (n = 51). In paired primary tissue samples and primary to recurrent/metastatic samples, at least 70% Luminal, HER2 enriched, and QNBC subtype did not change molecular profile. But, TNBC seems to be the "unstable" subtype. Within the total cohort, discordance in molecular profiles was identified in both synchronous (20%) and asynchronous (21%) intra-individual analyses. Irrespective of sample type, (Synchronous or Asynchronous), QNBC demonstrated higher concordant than TNBC. IHC and ISH results of the cancer related genes, demonstrated that gene/protein expression differ by molecular profile: TNBC (HR-/HER2-, AR+) and QNBC (HR-/HER2-, AR-). IHC in metastatic tumors, showed that the percentage of tumors positive of EGFR were higher, while PTEN and TLE3 were lower in QNBC compared to TNBC. Conclusion: Standard treatment of Breast Cancer (BC) relies on reliable assessment by IHC analysis of ER, PR, and HER2. Our analyses suggest that the heterogeneity of TNBC is at least partially associated with the presence or absence of AR expression, suggesting that QNBC should be considered as a clinically relevant BC subtype. IHC analysis of AR appears to be a practical assay to determine the most aggressive TNBC subtypes and identifies tumors that could benefit from available targeted therapies.
Language	English
Publishing date	2018-12-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233
ISSN	1936-5233
DOI	10.1016/j.tranon.2018.11.008
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Article ; Online: Thyroid hormone induction of human cholesterol 7 alpha-hydroxylase (Cyp7a1) in vitro.

Lammel Lindemann, Jan A / Angajala, Anusha / Engler, David A / Webb, Paul / Ayers, Stephen D

Molecular and cellular endocrinology

2014 Volume 388, Issue 1-2, Page(s) 32–40

Abstract: Thyroid hormone (TH) modulates serum cholesterol by acting on TH receptor β1 (TRβ1) in liver to regulate metabolic gene sets. In rodents, one important TH regulated step involves induction of Cyp7a1, an enzyme in the cytochrome P450 family, which ... ...

Abstract	Thyroid hormone (TH) modulates serum cholesterol by acting on TH receptor β1 (TRβ1) in liver to regulate metabolic gene sets. In rodents, one important TH regulated step involves induction of Cyp7a1, an enzyme in the cytochrome P450 family, which enhances cholesterol to bile acid conversion and plays a crucial role in regulation of serum cholesterol levels. Current models suggest, however, that Cyp7a1 has lost the capacity to respond to THs in humans. We were prompted to re-examine TH effects on cholesterol metabolic genes in human liver cells by a recent study of a synthetic TH mimetic which showed that serum cholesterol reductions were accompanied by increases in a marker for bile acid synthesis in humans. Here, we show that TH effects upon cholesterol metabolic genes are almost identical in mouse liver, mouse and human liver primary cells and human hepatocyte cell lines. Moreover, Cyp7a1 is a direct TR target gene that responds to physiologic TR levels through a set of distinct response elements in its promoter. These findings suggest that THs regulate cholesterol to bile acid conversion in similar ways in humans and rodent experimental models and that manipulation of hormone signaling pathways could provide a strategy to enhance Cyp7a1 activity in human patients.
MeSH term(s)	Adenoviridae/genetics ; Animals ; Base Sequence ; Cholesterol 7-alpha-Hydroxylase/genetics ; Cholesterol 7-alpha-Hydroxylase/metabolism ; Enzyme Induction ; Gene Expression ; HEK293 Cells ; Hep G2 Cells ; Humans ; Mice ; Promoter Regions, Genetic ; Protein Binding ; Thyroid Hormone Receptors beta/genetics ; Thyroid Hormone Receptors beta/metabolism ; Triiodothyronine/physiology
Chemical Substances	Thyroid Hormone Receptors beta ; Triiodothyronine (06LU7C9H1V) ; CYP7A1 protein, human (EC 1.14.14.23) ; Cholesterol 7-alpha-Hydroxylase (EC 1.14.14.23)
Language	English
Publishing date	2014-02-25
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2014.02.003
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Article ; Online: Genome-wide binding patterns of thyroid hormone receptor beta.

Ayers, Stephen / Switnicki, Michal Piotr / Angajala, Anusha / Lammel, Jan / Arumanayagam, Anithachristy S / Webb, Paul

PloS one

2014 Volume 9, Issue 2, Page(s) e81186

Abstract: Thyroid hormone (TH) receptors (TRs) play central roles in metabolism and are major targets for pharmaceutical intervention. Presently, however, there is limited information about genome wide localizations of TR binding sites. Thus, complexities of TR ... ...

Abstract	Thyroid hormone (TH) receptors (TRs) play central roles in metabolism and are major targets for pharmaceutical intervention. Presently, however, there is limited information about genome wide localizations of TR binding sites. Thus, complexities of TR genomic distribution and links between TRβ binding events and gene regulation are not fully appreciated. Here, we employ a BioChIP approach to capture TR genome-wide binding events in a liver cell line (HepG2). Like other NRs, TRβ appears widely distributed throughout the genome. Nevertheless, there is striking enrichment of TRβ binding sites immediately 5' and 3' of transcribed genes and TRβ can be detected near 50% of T3 induced genes. In contrast, no significant enrichment of TRβ is seen at negatively regulated genes or genes that respond to unliganded TRs in this system. Canonical TRE half-sites are present in more than 90% of TRβ peaks and classical TREs are also greatly enriched, but individual TRE organization appears highly variable with diverse half-site orientation and spacing. There is also significant enrichment of binding sites for TR associated transcription factors, including AP-1 and CTCF, near TR peaks. We conclude that T3-dependent gene induction commonly involves proximal TRβ binding events but that far-distant binding events are needed for T3 induction of some genes and that distinct, indirect, mechanisms are often at play in negative regulation and unliganded TR actions. Better understanding of genomic context of TR binding sites will help us determine why TR regulates genes in different ways and determine possibilities for selective modulation of TR action.
MeSH term(s)	Animals ; Binding Sites ; Cell Line ; Gene Expression Regulation ; Genome ; Hep G2 Cells ; Humans ; Ligands ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Multigene Family ; Oligonucleotide Array Sequence Analysis ; Plasmids/metabolism ; Protein Binding ; RNA/chemistry ; Response Elements ; Sequence Analysis, DNA ; Thyroid Hormone Receptors beta/metabolism
Chemical Substances	Ligands ; Thyroid Hormone Receptors beta ; RNA (63231-63-0)
Language	English
Publishing date	2014-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0081186
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Genome-wide binding patterns of thyroid hormone receptor beta.

Stephen Ayers / Michal Piotr Switnicki / Anusha Angajala / Jan Lammel / Anithachristy S Arumanayagam / Paul Webb

PLoS ONE, Vol 9, Iss 2, p e

2014 Volume 81186

Abstract	Thyroid hormone (TH) receptors (TRs) play central roles in metabolism and are major targets for pharmaceutical intervention. Presently, however, there is limited information about genome wide localizations of TR binding sites. Thus, complexities of TR genomic distribution and links between TRβ binding events and gene regulation are not fully appreciated. Here, we employ a BioChIP approach to capture TR genome-wide binding events in a liver cell line (HepG2). Like other NRs, TRβ appears widely distributed throughout the genome. Nevertheless, there is striking enrichment of TRβ binding sites immediately 5' and 3' of transcribed genes and TRβ can be detected near 50% of T3 induced genes. In contrast, no significant enrichment of TRβ is seen at negatively regulated genes or genes that respond to unliganded TRs in this system. Canonical TRE half-sites are present in more than 90% of TRβ peaks and classical TREs are also greatly enriched, but individual TRE organization appears highly variable with diverse half-site orientation and spacing. There is also significant enrichment of binding sites for TR associated transcription factors, including AP-1 and CTCF, near TR peaks. We conclude that T3-dependent gene induction commonly involves proximal TRβ binding events but that far-distant binding events are needed for T3 induction of some genes and that distinct, indirect, mechanisms are often at play in negative regulation and unliganded TR actions. Better understanding of genomic context of TR binding sites will help us determine why TR regulates genes in different ways and determine possibilities for selective modulation of TR action.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Thyroid hormone induction of human cholesterol 7 alpha-hydroxylase (Cyp7a1) in vitro

Lammel Lindemann, Jan A / Anusha Angajala / David A. Engler / Paul Webb / Stephen D. Ayers

Molecular and Cellular Endocrinology. 2014 May 05, v. 388

2014

Abstract: Thyroid hormone (TH) modulates serum cholesterol by acting on TH receptor Î²1 (TRÎ²1) in liver to regulate metabolic gene sets. In rodents, one important TH regulated step involves induction of Cyp7a1, an enzyme in the cytochrome P450 family, which ... ...

Abstract	Thyroid hormone (TH) modulates serum cholesterol by acting on TH receptor Î²1 (TRÎ²1) in liver to regulate metabolic gene sets. In rodents, one important TH regulated step involves induction of Cyp7a1, an enzyme in the cytochrome P450 family, which enhances cholesterol to bile acid conversion and plays a crucial role in regulation of serum cholesterol levels. Current models suggest, however, that Cyp7a1 has lost the capacity to respond to THs in humans. We were prompted to re-examine TH effects on cholesterol metabolic genes in human liver cells by a recent study of a synthetic TH mimetic which showed that serum cholesterol reductions were accompanied by increases in a marker for bile acid synthesis in humans. Here, we show that TH effects upon cholesterol metabolic genes are almost identical in mouse liver, mouse and human liver primary cells and human hepatocyte cell lines. Moreover, Cyp7a1 is a direct TR target gene that responds to physiologic TR levels through a set of distinct response elements in its promoter. These findings suggest that THs regulate cholesterol to bile acid conversion in similar ways in humans and rodent experimental models and that manipulation of hormone signaling pathways could provide a strategy to enhance Cyp7a1 activity in human patients.
Keywords	bile acids ; blood serum ; cholesterol ; cytochrome P-450 ; genes ; hepatocytes ; humans ; liver ; mice ; models ; patients ; promoter regions ; response elements ; signal transduction ; thyroid hormones
Language	English
Dates of publication	2014-0505
Size	p. 32-40.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2014.02.003
Database	NAL-Catalogue (AGRICOLA)

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