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Article ; Online: Chromatin Organization and Transcriptional Programming of Breast Cancer Cell Identity.

Bobbitt, Jessica R / Seachrist, Darcie D / Keri, Ruth A

2023 Volume 164, Issue 8

Abstract: The advent of sequencing technologies for assessing chromosome conformations has provided a wealth of information on the organization of the 3-dimensional genome and its role in cancer progression. It is now known that changes in chromatin folding and ... ...

Abstract	The advent of sequencing technologies for assessing chromosome conformations has provided a wealth of information on the organization of the 3-dimensional genome and its role in cancer progression. It is now known that changes in chromatin folding and accessibility can promote aberrant activation or repression of transcriptional programs that can drive tumorigenesis and progression in diverse cancers. This includes breast cancer, which comprises several distinct subtypes defined by their unique transcriptomes that dictate treatment response and patient outcomes. Of these, basal-like breast cancer is an aggressive subtype controlled by a pluripotency-enforcing transcriptome. Meanwhile, the more differentiated luminal subtype of breast cancer is driven by an estrogen receptor-dominated transcriptome that underlies its responsiveness to antihormone therapies and conveys improved patient outcomes. Despite the clear differences in molecular signatures, the genesis of each subtype from normal mammary epithelial cells remains unclear. Recent technical advances have revealed key distinctions in chromatin folding and organization between subtypes that could underlie their transcriptomic and, hence, phenotypic differences. These studies also suggest that proteins controlling particular chromatin states may be useful targets for treating aggressive disease. In this review, we explore the current state of understanding of chromatin architecture in breast cancer subtypes and its potential role in defining their phenotypic characteristics.
MeSH term(s)	Humans ; Female ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Breast/metabolism ; Chromatin/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic
Chemical Substances	Chromatin
Language	English
Publishing date	2023-07-11
Publishing country	United States
Document type	Review ; 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/endocr/bqad100
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Article ; Online: The Activin Social Network: Activin, Inhibin, and Follistatin in Breast Development and Cancer.

Seachrist, Darcie D / Keri, Ruth A

Endocrinology

2019 Volume 160, Issue 5, Page(s) 1097–1110

Abstract: Activins and inhibins are closely related protein heterodimers with a similar tissue distribution; however, these two complexes have opposing functions in development and disease. Both are secreted cytokine hormones, with activin the primary inducer of ... ...

Abstract	Activins and inhibins are closely related protein heterodimers with a similar tissue distribution; however, these two complexes have opposing functions in development and disease. Both are secreted cytokine hormones, with activin the primary inducer of downstream signaling cascades and inhibin acting as a rheostat that exquisitely governs activin function. Adding to the complexity of activin signaling, follistatin, a highly glycosylated monomeric protein, binds activin with high affinity and restrains downstream pathway activation but through a mechanism distinct from that of inhibin. These three proteins were first identified as key ovarian hormones in the pituitary-gonadal axis that direct the synthesis and secretion of FSH from the pituitary, hence controlling folliculogenesis. Research during the past 30 years has expanded the roles of these proteins, first by discovering the ubiquitous expression of the trio and then by implicating them in a wide array of biological functions. In concert, these three hormones govern tissue development, homeostasis, and disease in multiple organ systems through diverse autocrine and paracrine mechanisms. In the present study, we have reviewed the actions of activin and its biological inhibitors, inhibin, and follistatin, in mammary gland morphogenesis and cancer.
MeSH term(s)	Activins/genetics ; Activins/metabolism ; Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; Follistatin/genetics ; Follistatin/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Inhibins/genetics ; Inhibins/metabolism ; Mammary Glands, Human/metabolism ; Signal Transduction
Chemical Substances	Follistatin ; Activins (104625-48-1) ; Inhibins (57285-09-3)
Language	English
Publishing date	2019-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2019-00015
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Article ; Online: Up to your NEK2 in CIN.

Seachrist, Darcie D / Anstine, Lindsey J / Keri, Ruth A

Oncotarget

2021 Volume 12, Issue 8, Page(s) 723–725

Language	English
Publishing date	2021-04-13
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.27918
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Article: FOXA1: A Pioneer of Nuclear Receptor Action in Breast Cancer.

Seachrist, Darcie D / Anstine, Lindsey J / Keri, Ruth A

Cancers

2021 Volume 13, Issue 20

Abstract: The pioneering function of FOXA1 establishes estrogen-responsive transcriptomes in luminal breast cancer. Dysregulated FOXA1 chromatin occupancy through focal amplification, mutation, or cofactor recruitment modulates estrogen receptor (ER) ... ...

Abstract	The pioneering function of FOXA1 establishes estrogen-responsive transcriptomes in luminal breast cancer. Dysregulated FOXA1 chromatin occupancy through focal amplification, mutation, or cofactor recruitment modulates estrogen receptor (ER) transcriptional programs and drives endocrine-resistant disease. However, ER is not the sole nuclear receptor (NR) expressed in breast cancers, nor is it the only NR for which FOXA1 serves as a licensing factor. Receptors for androgens, glucocorticoids, and progesterone are also found in the majority of breast cancers, and their functions are also impacted by FOXA1. These NRs interface with ER transcriptional programs and, depending on their activation level, can reprogram FOXA1-ER cistromes. Thus, NR interplay contributes to endocrine therapy response and resistance and may provide a vulnerability for future therapeutic benefit in patients. Herein, we review what is known regarding FOXA1 regulation of NR function in breast cancer in the context of cell identity, endocrine resistance, and NR crosstalk in breast cancer progression and treatment.
Language	English
Publishing date	2021-10-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13205205
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Article ; Online: The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer.

Pai, Chun-Peng / Wang, Han / Seachrist, Darcie D / Agarwal, Neel / Adams, Joshua A / Liu, Zhenghao / Keri, Ruth A / Cao, Kaixiang / Schiemann, William P / Kao, Hung-Ying

Cell death and differentiation

2024

Abstract: The alternative splicing of PML precursor mRNA gives rise to various PML isoforms, yet their expression profile in breast cancer cells remains uncharted. We discovered that PML1 is the most abundant isoform in all breast cancer subtypes, and its ... ...

Abstract	The alternative splicing of PML precursor mRNA gives rise to various PML isoforms, yet their expression profile in breast cancer cells remains uncharted. We discovered that PML1 is the most abundant isoform in all breast cancer subtypes, and its expression is associated with unfavorable prognosis in estrogen receptor-positive (ER+) breast cancers. PML depletion reduces cell proliferation, invasion, and stemness, while heterologous PML1 expression augments these processes and fuels tumor growth and resistance to fulvestrant, an FDA-approved drug for ER+ breast cancer, in a mouse model. Moreover, PML1, rather than the well-known tumor suppressor isoform PML4, rescues the proliferation of PML knockdown cells. ChIP-seq analysis reveals significant overlap between PML-, ER-, and Myc-bound promoters, suggesting their coordinated regulation of target gene expression, including genes involved in breast cancer stem cells (BCSCs), such as JAG1, KLF4, YAP1, SNAI1, and MYC. Loss of PML reduces BCSC-related gene expression, and exogenous PML1 expression elevates their expression. Consistently, PML1 restores the association of PML with these promoters in PML-depleted cells. We identified a novel association between PML1 and WDR5, a key component of H3K4 methyltransferase (HMTs) complexes that catalyze H3K4me1 and H3K4me3. ChIP-seq analyses showed that the loss of PML1 reduces H3K4me3 in numerous loci, including BCSC-associated gene promoters. Additionally, PML1, not PML4, re-establishes the H3K4me3 mark on these promoters in PML-depleted cells. Significantly, PML1 is essential for recruiting WDR5, MLL1, and MLL2 to these gene promoters. Inactivating WDR5 by knockdown or inhibitors phenocopies the effects of PML1 loss, reducing BCSC-related gene expression and tumorsphere formation and enhancing fulvestrant's anticancer activity. Our findings challenge the conventional understanding of PML as a tumor suppressor, redefine its role as a promoter of tumor growth in breast cancer, and offer new insights into the unique roles of PML isoforms in breast cancer.
Language	English
Publishing date	2024-04-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-024-01294-6
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Article ; Online: Disruption of CDK7 signaling leads to catastrophic chromosomal instability coupled with a loss of condensin-mediated chromatin compaction.

Piemonte, Katrina M / Webb, Bryan M / Bobbitt, Jessica R / Majmudar, Parth R / Cuellar-Vite, Leslie / Bryson, Benjamin L / Latina, Nicholas C / Seachrist, Darcie D / Keri, Ruth A

The Journal of biological chemistry

2023 Volume 299, Issue 7, Page(s) 104834

Abstract: Chromatin organization is highly dynamic and modulates DNA replication, transcription, and chromosome segregation. Condensin is essential for chromosome assembly during mitosis and meiosis, as well as maintenance of chromosome structure during interphase. ...

Abstract	Chromatin organization is highly dynamic and modulates DNA replication, transcription, and chromosome segregation. Condensin is essential for chromosome assembly during mitosis and meiosis, as well as maintenance of chromosome structure during interphase. While it is well established that sustained condensin expression is necessary to ensure chromosome stability, the mechanisms that control its expression are not yet known. Herein, we report that disruption of cyclin-dependent kinase 7 (CDK7), the core catalytic subunit of CDK-activating kinase, leads to reduced transcription of several condensin subunits, including structural maintenance of chromosomes 2 (SMC2). Live and static microscopy revealed that inhibiting CDK7 signaling prolongs mitosis and induces chromatin bridge formation, DNA double-strand breaks, and abnormal nuclear features, all of which are indicative of mitotic catastrophe and chromosome instability. Affirming the importance of condensin regulation by CDK7, genetic suppression of the expression of SMC2, a core subunit of this complex, phenocopies CDK7 inhibition. Moreover, analysis of genome-wide chromatin conformation using Hi-C revealed that sustained activity of CDK7 is necessary to maintain chromatin sublooping, a function that is ascribed to condensin. Notably, the regulation of condensin subunit gene expression is independent of superenhancers. Together, these studies reveal a new role for CDK7 in sustaining chromatin configuration by ensuring the expression of condensin genes, including SMC2.
MeSH term(s)	Chromatin/genetics ; Chromatin/metabolism ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Mitosis/genetics ; Chromosomal Instability/genetics ; Signal Transduction ; Humans ; Cell Line, Tumor ; Gene Expression Regulation/genetics ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Gene Silencing
Chemical Substances	Chromatin ; condensin complexes ; Cyclin-Dependent Kinases (EC 2.7.11.22) ; CDK7 protein, human ; SMC2 protein, human ; Cell Cycle Proteins
Language	English
Publishing date	2023-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.104834
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Article ; Online: TGF-β/activin signaling promotes CDK7 inhibitor resistance in triple-negative breast cancer cells through upregulation of multidrug transporters.

Webb, Bryan M / Bryson, Benjamin L / Williams-Medina, Eduardo / Bobbitt, Jessica R / Seachrist, Darcie D / Anstine, Lindsey J / Keri, Ruth A

The Journal of biological chemistry

2021 Volume 297, Issue 4, Page(s) 101162

Abstract: Cyclin-dependent kinase 7 (CDK7) is a master regulatory kinase that drives cell cycle progression and stimulates expression of oncogenes in a myriad of cancers. Inhibitors of CDK7 (CDK7i) are currently in clinical trials; however, as with many cancer ... ...

Abstract	Cyclin-dependent kinase 7 (CDK7) is a master regulatory kinase that drives cell cycle progression and stimulates expression of oncogenes in a myriad of cancers. Inhibitors of CDK7 (CDK7i) are currently in clinical trials; however, as with many cancer therapies, patients will most likely experience recurrent disease due to acquired resistance. Identifying targets underlying CDK7i resistance will facilitate prospective development of new therapies that can circumvent such resistance. Here we utilized triple-negative breast cancer as a model to discern mechanisms of resistance as it has been previously shown to be highly responsive to CDK7 inhibitors. After generating cell lines with acquired resistance, high-throughput RNA sequencing revealed significant upregulation of genes associated with efflux pumps and transforming growth factor-beta (TGF-β) signaling pathways. Genetic silencing or pharmacological inhibition of ABCG2, an efflux pump associated with multidrug resistance, resensitized resistant cells to CDK7i, indicating a reliance on these transporters. Expression of activin A (INHBA), a member of the TGF-β family of ligands, was also induced, whereas its intrinsic inhibitor, follistatin (FST), was repressed. In resistant cells, increased phosphorylation of SMAD3, a downstream mediator, confirmed an increase in activin signaling, and phosphorylated SMAD3 directly bound the ABCG2 promoter regulatory region. Finally, pharmacological inhibition of TGF-β/activin receptors or genetic silencing of SMAD4, a transcriptional partner of SMAD3, reversed the upregulation of ABCG2 in resistant cells and phenocopied ABCG2 inhibition. This study reveals that inhibiting the TGF-β/Activin-ABCG2 pathway is a potential avenue for preventing or overcoming resistance to CDK7 inhibitors.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily G, Member 2/biosynthesis ; ATP Binding Cassette Transporter, Subfamily G, Member 2/genetics ; Cell Line, Tumor ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Inhibin-beta Subunits/genetics ; Inhibin-beta Subunits/metabolism ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Protein Kinase Inhibitors/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Up-Regulation/drug effects
Chemical Substances	ABCG2 protein, human ; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; Neoplasm Proteins ; Protein Kinase Inhibitors ; Transforming Growth Factor beta ; inhibin beta A subunit ; Inhibin-beta Subunits (93443-12-0) ; Cyclin-Dependent Kinases (EC 2.7.11.22) ; cyclin-dependent kinase-activating kinase (EC 2.7.11.22)
Language	English
Publishing date	2021-09-02
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	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2021.101162
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Article ; Online: TLE3 Sustains Luminal Breast Cancer Lineage Fidelity to Suppress Metastasis.

Anstine, Lindsey J / Majmudar, Parth R / Aponte, Amy / Singh, Salendra / Zhao, Ran / Weber-Bonk, Kristen L / Abdul-Karim, Fadi W / Valentine, Mitchell / Seachrist, Darcie D / Grennel-Nickelson, Katelyn E / Cuellar-Vite, Leslie / Sizemore, Gina M / Sizemore, Steven T / Webb, Bryan M / Thompson, Cheryl L / Keri, Ruth A

Cancer research

2023 Volume 83, Issue 7, Page(s) 997–1015

Abstract: Breast cancer subtypes and their phenotypes parallel different stages of the mammary epithelial cell developmental hierarchy. Discovering mechanisms that control lineage identity could provide novel avenues for mitigating disease progression. Here we ... ...

Abstract	Breast cancer subtypes and their phenotypes parallel different stages of the mammary epithelial cell developmental hierarchy. Discovering mechanisms that control lineage identity could provide novel avenues for mitigating disease progression. Here we report that the transcriptional corepressor TLE3 is a guardian of luminal cell fate in breast cancer and operates independently of the estrogen receptor. In luminal breast cancer, TLE3 actively repressed the gene-expression signature associated with highly aggressive basal-like breast cancers (BLBC). Moreover, maintenance of the luminal lineage depended on the appropriate localization of TLE3 to its transcriptional targets, a process mediated by interactions with FOXA1. By repressing genes that drive BLBC phenotypes, including SOX9 and TGFβ2, TLE3 prevented the acquisition of a hybrid epithelial-mesenchymal state and reduced metastatic capacity and aggressive cellular behaviors. These results establish TLE3 as an essential transcriptional repressor that sustains the more differentiated and less metastatic nature of luminal breast cancers. Approaches to induce TLE3 expression could promote the acquisition of less aggressive, more treatable disease states to extend patient survival. Significance: Transcriptional corepressor TLE3 actively suppresses SOX9 and TGFβ transcriptional programs to sustain the luminal lineage identity of breast cancer cells and to inhibit metastatic progression.
MeSH term(s)	Cell Differentiation ; Co-Repressor Proteins/genetics ; Neoplasms ; Receptors, Estrogen/metabolism ; Transcription Factors ; Transforming Growth Factor beta ; Breast Neoplasms/metabolism ; Humans
Chemical Substances	Co-Repressor Proteins ; Receptors, Estrogen ; Transcription Factors ; Transforming Growth Factor beta
Language	English
Publishing date	2023-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; 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-22-3133
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Article ; Online: GABA(A) receptor pi (GABRP) stimulates basal-like breast cancer cell migration through activation of extracellular-regulated kinase 1/2 (ERK1/2).

Sizemore, Gina M / Sizemore, Steven T / Seachrist, Darcie D / Keri, Ruth A

The Journal of biological chemistry

2014 Volume 289, Issue 35, Page(s) 24102–24113

Abstract: Breast cancer is a heterogeneous disease comprised of distinct subtypes predictive of patient outcome. Tumors of the basal-like subtype have a poor prognosis due to inherent aggressiveness and the lack of targeted therapeutics. Basal-like tumors ... ...

Abstract	Breast cancer is a heterogeneous disease comprised of distinct subtypes predictive of patient outcome. Tumors of the basal-like subtype have a poor prognosis due to inherent aggressiveness and the lack of targeted therapeutics. Basal-like tumors typically lack estrogen receptor-α, progesterone receptor and HER2/ERBB2, or in other words they are triple negative (TN). Continued evaluation of basal-like breast cancer (BLBC) biology is essential to identify novel therapeutic targets. Expression of the pi subunit of the GABA(A) receptor (GABRP) is associated with the BLBC/TN subtype, and herein, we reveal its expression also correlates with metastases to the brain and poorer patient outcome. GABRP expression in breast cancer cell lines also demonstrates a significant correlation with the basal-like subtype suggesting that GABRP functions in the initiation and/or progression of basal-like tumors. To address this postulate, we stably silenced GABRP in two BLBC cell lines, HCC1187 and HCC70 cells. Decreased GABRP reduces in vitro tumorigenic potential and migration concurrent with alterations in the cytoskeleton, specifically diminished cellular protrusions and expression of the BLBC-associated cytokeratins, KRT5, KRT6B, KRT14, and KRT17. Silencing GABRP also decreases phosphorylation of extracellular regulated kinase 1/2 (ERK1/2) in both cell lines and selective inhibition of ERK1/2 similarly decreases the basal-like cytokeratins as well as migration. Combined, these data reveal a GABRP-ERK1/2-cytokeratin axis that maintains the migratory phenotype of basal-like breast cancer. GABRP is a component of a cell surface receptor, thus, these findings suggest that targeting this new signaling axis may have therapeutic potential in BLBC.
MeSH term(s)	Breast Neoplasms/enzymology ; Breast Neoplasms/pathology ; Cell Line ; Enzyme Activation ; Gene Expression Profiling ; Gene Silencing ; Humans ; MAP Kinase Signaling System ; Real-Time Polymerase Chain Reaction ; Receptors, GABA-A/genetics ; Receptors, GABA-A/physiology ; Survival Analysis
Chemical Substances	GABRP protein, human ; Receptors, GABA-A
Language	English
Publishing date	2014-07-10
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	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M114.593582
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Article ; Online: Correction: Bromodomain and extraterminal protein inhibition blocks growth of triple-negative breast cancers through the suppression of aurora kinases.

Sahni, Jennifer M / Gayle, Sylvia S / Bonk, Kristen L Weber / Vite, Leslie Cuellar / Yori, Jennifer L / Webb, Bryan / Ramos, Erika K / Seachrist, Darcie D / Landis, Melissa D / Chang, Jenny C / Bradner, James E / Keri, Ruth A

The Journal of biological chemistry

2020 Volume 295, Issue 27, Page(s) 9266

Language	English
Publishing date	2020-06-29
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.AAC120.014699
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