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4. TLE3 Sustains Luminal Breast Cancer Lineage Fidelity to Suppress Metastasis

Author

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

Published
2023
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5. UbcH7 regulates 53BP1 stability and DSB repair

Author

Han, Xiangzi, Zhang, Lei, Chung, Jinsil, Pozo, Franklin Mayca, Tran, Amanda, Seachrist, Darcie D., Jacobberger, James W., Keri, Ruth A., Gilmore, Hannah, and Zhang, Youwei

Published
2014

10. Additional file 2 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 2: Figure S2. Identification of a KLF4-regulated protein signature reveals EGFR as a downstream target. The top a 63 downregulated proteins and b 14 upregulated proteins after KLF4 overexpression. c Protein-Protein interaction network including proteins with greater than 2-fold expression decrease after AdKLF4 infection and RPPA analysis. Colored nodes indicate query proteins and the first shell of interactors. Teal and purple lines indicate known interactions. Green, red, yellow and blue lines indicate predicted interactions. d REVERT staining of total protein in MDA-MB-231 cells after transduction with AdGFP (AdG) or AdKLF4 (AdK).

Published
2020
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11. Additional file 3 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 3: Figure S3. KLF4 negatively regulates the EGFR signaling pathway. a REVERT staining of total protein in Fig. 3a. b REVERT staining of total protein in Fig. 3c. c REVERT staining of total protein in Fig. 3e.

Published
2020
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12. Additional file 1 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Subjects
skin and connective tissue diseases
Abstract

Additional file 1: Figure S1. KLF4 represses migration, invasion, and cell growth in breast epithelial cells. a REVERT staining of total protein across eight different breast cell lines: MCF10A (10A), MCF7, T47D, SKBR3, SUM159, HCC70, MDA-MB-468 (468), and MDA-MB-231 (231). b REVERT staining of total protein in MCF10A cells as well as MDA-MB-231 and MDA-MB-468 after transduction with AdGFP (G) or AdKLF4 (K). c REVERT staining of total protein in MCF10A cells after transfection with siNS or siKLF4 (siK).

Published
2020
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13. Additional file 5 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 5: Table S1. ChIP-PCR primer sequences. Primer sequences targeting six regions within the EGFR promoter are listed.

Published
2020
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14. Additional file 4 of KLF4 defines the efficacy of the epidermal growth factor receptor inhibitor, erlotinib, in triple-negative breast cancer cells by repressing the EGFR gene

Author

Melyssa S. Roberts, Anstine, Lindsey J., Finke, Viviane S., Bryson, Benjamin L., Webb, Bryan M., Weber-Bonk, Kristen L., Seachrist, Darcie D., Parth R. Majmudar, and Keri, Ruth A.

Abstract

Additional file 4: Figure S4. Repression of EGFR is an obligatory intermediate step for KLF4 to inhibit aggressive breast cancer phenotypes. a REVERT staining of total protein in Fig. 5a. b REVERT staining of total protein in Fig. 5b.

Published
2020
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16. The transcriptional repressor BCL11A promotes breast cancer metastasis

Author

Seachrist, Darcie D., primary, Hannigan, Molly M., additional, Ingles, Natasha N., additional, Webb, Bryan M., additional, Weber-Bonk, Kristen L., additional, Yu, Peng, additional, Bebek, Gurkan, additional, Singh, Salendra, additional, Sizemore, Steven T., additional, Varadan, Vinay, additional, Licatalosi, Donny D., additional, and Keri, Ruth A., additional

Published
2020
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17. Correction: Bromodomain and extraterminal protein inhibition blocks growth of triple-negative breast cancers through the suppression of aurora kinases.

Author

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

Published
2020
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18. LIN9 and NEK2 Are Core Regulators of Mitotic Fidelity That Can Be Therapeutically Targeted to Overcome Taxane Resistance

Author

Roberts, Melyssa S., primary, Sahni, Jennifer M., additional, Schrock, Morgan S., additional, Piemonte, Katrina M., additional, Weber-Bonk, Kristen L., additional, Seachrist, Darcie D., additional, Avril, Stefanie, additional, Anstine, Lindsey J., additional, Singh, Salendra, additional, Sizemore, Steven T., additional, Varadan, Vinay, additional, Summers, Matthew K., additional, and Keri, Ruth A., additional

Published
2020
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21. Mitotic Vulnerability in Triple-Negative Breast Cancer Associated with LIN9 Is Targetable with BET Inhibitors

Author

Sahni, Jennifer M., primary, Gayle, Sylvia S., additional, Webb, Bryan M., additional, Weber-Bonk, Kristen L., additional, Seachrist, Darcie D., additional, Singh, Salendra, additional, Sizemore, Steven T., additional, Restrepo, Nicole A., additional, Bebek, Gurkan, additional, Scacheri, Peter C., additional, Varadan, Vinay, additional, Summers, Matthew K., additional, and Keri, Ruth A., additional

Published
2017
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23. Bromodomain and Extraterminal Protein Inhibition Blocks Growth of Triple-negative Breast Cancers through the Suppression of Aurora Kinases

Author

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

Published
2016
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24. Krüppel-like Factor 4 Inhibits Tumorigenic Progression and Metastasis in a Mouse Model of Breast Cancer12

Author

Yori, Jennifer L, Seachrist, Darcie D, Johnson, Emhonta, Lozada, Kristen L, Abdul-Karim, Fadi W, Chodosh, Lewis A, Schiemann, William P, and Keri, Ruth A

Subjects
Mice, Inbred BALB C, Epithelial-Mesenchymal Transition, fungi, Carcinoma, Kruppel-Like Transcription Factors, Breast Neoplasms, Mice, Transgenic, Xenograft Model Antitumor Assays, Gene Expression Regulation, Neoplastic, Disease Models, Animal, Kruppel-Like Factor 4, Mice, stomatognathic system, embryonic structures, Disease Progression, Animals, Humans, Female, Genes, Tumor Suppressor, sense organs, biological phenomena, cell phenomena, and immunity, Neoplasm Metastasis, Cells, Cultured, Research Article
Abstract

Krüppel-like factor 4 (KLF4) is a zinc finger transcription factor that functions as an oncogene or tumor suppressor in a highly tissue-specific cell-dependent manner. However, its precise role in breast cancer and metastasis remains unclear. Here, we show that transient adenoviral expression of KLF4 in the 4T1 orthotopic mammary cancer model significantly attenuated primary tumor growth as well as micrometastases to the lungs and liver. These results can be attributed, in part, to decreased proliferation and increased apoptosis. Further supporting a tumor-suppressive role for KLF4 in the breast, we found that KLF4 expression is lost in a mouse model of HER2/NEU/ERBB2-positive breast cancer. To determine whether enforced KLF4 expression could alter tumor latency in these mice, we used a doxycycline-inducible expression model in the context of the MMTV-Neu transgene. Surprisingly, tumors that developed in this model also lost KLF4 expression, suggesting negative selection for sustained expression. We have previously reported that KLF4 inhibits epithelial-to-mesenchymal transition (EMT), a preliminary step in metastatic progression. Overexpression of KLF4 in 4T1 cells led to a significant reduction in the expression of Snail, a key mediator of EMT and metastasis. Conversely, KLF4 silencing increased Snail expression in the nontransformed MCF-10A cell line. Collectively, these data demonstrate the first functional, in vivo evidence for KLF4 as a tumor suppressor in breast cancer cells. Furthermore, our findings suggest an inhibitory role for KLF4 during breast cancer metastases that functions, in part, through repression of Snail.

Published
2011

25. Aberrant expression of LMO4 induces centrosome amplification and mitotic spindle abnormalities in breast cancer cells

Author

Montañez-Wiscovich, Marjorie E., Shelton, Melissa D., Seachrist, Darcie D., Lozada, Kristen L., Johnson, Emhonta J., Miedler, John D., Abdul-Karim, Fadi W., Visvader, Jane E., and Keri, Ruth A.

Subjects
Centrosome, Homeodomain Proteins, Cell Cycle, Genes, BRCA1, Breast Neoplasms, Spindle Apparatus, LIM Domain Proteins, Article, Neoplasm Proteins, Receptors, Estrogen, Mutation, Mitotic Index, Humans, Female, RNA, Messenger, RNA, Neoplasm, Adaptor Proteins, Signal Transducing, Transcription Factors
Abstract

The LIM-only protein, LMO4, is a transcriptional modulator overexpressed in breast cancer. It is oncogenic in murine mammary epithelium and is required for G2/M progression of ErbB2-dependent cells as well as growth and invasion of other breast cancer cell types. However, the mechanisms underlying the oncogenic activity of LMO4 remain unclear. Herein, we show that LMO4 is expressed in all breast cancer subtypes examined and its expression level correlates with the degree of proliferation of such tumours. In addition, we have determined that LMO4 silencing induces G2/M arrest in cells from various breast cancer subtypes, suggesting that LMO4 action in the cell cycle is not restricted to a single breast cancer subtype. This arrest was accompanied by increased cell death, amplification of centrosomes, and formation of abnormal mitotic spindles. Consistent with its ability to positively and negatively regulate the formation of active transcription complexes, overexpression of LMO4 also resulted in an increase in centrosome number. Centrosome amplification has been shown to prolong the G2/M phase of the cell cycle and induce apoptosis; thus, we conclude that supernumerary centrosomes mediate the G2/M arrest and cell death in LMO4-deficient cells. Furthermore, the correlation of centrosome amplification with genomic instability suggests that the impact of dysregulated LMO4 on the centrosome cycle may promote LMO4-induced tumour formation.

Published
2010

36. UbcH7 regulates 53BP1 stability and DSB repair.

Author

Xiangzi Han, Lei Zhang, Jinsil Chung, Pozo, Franklin Mayca, Tran, Amanda, Seachrist, Darcie D., Jacobberger, James W., Keri, Ruth A., Gilmore, Hannah, and Youwei Zhang

Subjects
UBIQUITIN-conjugating enzymes, DNA repair, TUMOR suppressor proteins, UBIQUITINATION, PROTEASOMES
Abstract

DNA double-strand break (DSB) repair is not only key to genome stability but is also an important anticancer target. Through an shRNA library-based screening, we identified ubiquitin-conjugating enzyme H7 (UbcH7, also known as Ube2L3), a ubiquitin E2 enzyme, as a critical player in DSB repair. UbcH7 regulates both the steady-state and replicative stress-induced ubiquitination and proteasome-dependent degradation of the tumor suppressor p53-binding protein 1 (53BP1). Phosphorylation of 53BP1 at the N terminus is involved in the replicative stress-induced 53BP1 degradation. Depletion of UbcH7 stabilizes 53BP1, leading to inhibition of DSB end resection. Therefore, UbcH7-depleted cells display increased nonhomologous end-joining and reduced homologous recombination for DSB repair. Accordingly, UbcH7-depleted cells are sensitive to DNA damage likely because they mainly used the error-prone nonhomologous end-joining pathway to repair DSBs. Our studies reveal a novel layer of regulation of the DSB repair choice and propose an innovative approach to enhance the effect of radiotherapy or chemotherapy through stabilizing 53BP1. [ABSTRACT FROM AUTHOR]

Published
2014
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38. Embryonic expression of the luteinizing hormone beta gene appears to be coupled to the transient appearance of p8, a high mobility group-related transcription factor.

Author

Quirk CC, Seachrist DD, and Nilson JH

Subjects
Cell Line, Gene Silencing, High Mobility Group Proteins genetics, Polymerase Chain Reaction, Up-Regulation physiology, Embryo, Mammalian metabolism, Embryo, Nonmammalian, Gene Expression Regulation, Developmental physiology, High Mobility Group Proteins physiology, Luteinizing Hormone, beta Subunit genetics
Abstract

A comparison between two pituitary-derived cell lines (alpha T3-1 and L beta T2) that represent gonadotropes at early and late stages of development, respectively, was performed to further elucidate the genomic repertoire required for gonadotrope specification and luteinizing hormone beta (LH beta) gene expression. One isolated clone that displayed higher expression levels in L beta T2 cells encodes p8, a high mobility group-like protein with mitogenic potential that is up-regulated in response to proapoptotic stimuli and in some developing tissues. To test the functional significance of this factor in developing gonadotropes, a knockdown of p8 in L beta T2 cells was generated. The loss of p8 mRNA correlated with loss of endogenous LH beta mRNA and the loss of activity of a transfected LH beta promoter-driven reporter, even upon treatment with gonadotropin-releasing hormone. In addition, expression of p8 mRNA in developing mouse pituitary glands mirrored its expression in the gonadotrope-derived cell lines and coincided with the first detectable appearance of LH beta mRNA. In contrast, p8 mRNA was undetectable in the pituitary glands of normal adults. Taken together, our data indicate that p8 is a stage-specific component of the gonadotrope transcriptome that may play a functional role in the initiation of LH beta gene expression during embryonic cellular differentiation.

Published
2003
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