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Start Over Author "Tony Zhu" Journal journal of biological chemistry
4 results on '"Tony Zhu"'

1. PRIP Promotes Tumor Formation through Enhancing Serum-responsive Factor-mediated FOS Expression

Author

Liping Hu, Yi Jun Zhu, Chao Qi, and Yiwei Tony Zhu

Subjects
Serum Response Factor, Nuclear Receptor Coactivators, Mammary Neoplasms, Animal, Biology, medicine.disease_cause, Methylation, Biochemistry, Histones, Mice, Cell Line, Tumor, Neoplasms, Gene expression, Coactivator, Serum response factor, medicine, Animals, Humans, Transcription, Chromatin, and Epigenetics, Promoter Regions, Genetic, Molecular Biology, Cell Proliferation, Mice, Knockout, Regulation of gene expression, Mammary tumor, Lysine, Intracellular Signaling Peptides and Proteins, Cell Biology, Gene Expression Regulation, Neoplastic, Nuclear receptor, ras Proteins, Cancer research, Female, Carcinogenesis, Proto-Oncogene Proteins c-fos, Chromatin immunoprecipitation, Protein Binding
Abstract

PRIP (peroxisome proliferator-activator receptor interacting protein) is a nuclear receptor coactivator required for mammary gland development. To understand the function of PRIP in breast tumorigenesis, we established a mammary tumor cell line with the PRIPLoxp/Loxp genotype. By knocking out the PRIP gene in the tumor cell line, we demonstrated that PRIP deficiency led to inhibited tumor formation without affecting tumor cell proliferation. The PRIP deficiency was associated with decreased cell invasion and migration capabilities. We found that PRIP deficiency substantially reduced FOS gene expression. A chromatin immunoprecipitation assay revealed that PRIP was recruited to the FOS promoter. In addition, we demonstrated that PRIP also directly up-regulated the FOS gene expression in human breast cancer cells. Promoter analysis showed that PRIP acted through serum-responsive factor to regulate FOS gene expression. Finally, by re-expressing the FOS gene, we confirmed that the inhibited tumor formation of PRIP-deficient tumor cells was due to reduced expression of the FOS gene.

Published
2009

2. Null Mutation of Peroxisome Proliferator-activated Receptor-interacting Protein in Mammary Glands Causes Defective Mammopoiesis

Author

Yi Jun Zhu, Papreddy Kashireddy, Yiwei Tony Zhu, Sambasiva Rao, and Chao Qi

Subjects
EGF Family of Proteins, medicine.medical_specialty, Proliferation index, Nuclear Receptor Coactivators, Gene Expression, Apoptosis, Mice, Transgenic, Amphiregulin, Biochemistry, Mice, Mammary Glands, Animal, stomatognathic system, Pregnancy, Mammary tumor virus, Internal medicine, Lactation, Adipocytes, medicine, Animals, RNA, Messenger, Sexual Maturation, Betacellulin, Molecular Biology, Glycoproteins, Mice, Knockout, biology, Intracellular Signaling Peptides and Proteins, Myoepithelial cell, Wild type, Caseins, Epithelial Cells, Estrogens, Cell Biology, Transforming Growth Factor alpha, Milk Proteins, Whey Proteins, Endocrinology, medicine.anatomical_structure, Mammary Tumor Virus, Mouse, Mutation, biology.protein, Intercellular Signaling Peptides and Proteins, Female, Whey Acidic Protein, Carrier Proteins, Cell Division
Abstract

To investigate the role of nuclear receptor coactivator peroxisome proliferator-activated receptor-interacting protein (PRIP) in mammary gland development, we generated a conditional null mutation of PRIP in mammary glands. In PRIP-deficient mammary glands, the elongation of ducts during puberty was not affected, but the numbers of ductal branches were decreased, a condition that persisted long after puberty, indicating that the potential of ductal branching was impaired. During pregnancy, PRIP-deficient mammary glands exhibited decreased alveolar density. The lactating PRIP-deficient glands contained scant lobuloalveoli with many adipocytes, whereas the wild type glands were composed of virtually no adipocytes but mostly lobuloalveoli. As a result, PRIP mammary-deficient glands could not produce enough milk to nurse all the pups during lactation. The ductal branching of mammary glands in response to estrogen treatment was attenuated in PRIP mutant glands. Whereas the proliferation index was similar between wild type and PRIP-deficient glands, increased apoptosis was observed in PRIP-deficient glands. PRIP-deficient glands expressed increased amphiregulin, transforming growth factor-alpha, and betacellulin mRNA as compared with wild type glands. The differentiated function of PRIP-deficient mammary epithelial cells was largely intact, as evidenced by the expression of abundant beta-casein, whey acidic protein (WAP), and WDNM1 mRNA. We conclude that PRIP is important for normal mammary gland development.

Published
2004

3. Absent, Small or Homeotic 2-like Protein (ASH2L) Enhances the Transcription of the Estrogen Receptor α Gene through GATA-binding Protein 3 (GATA3).

Author

Jin Qi, Lei Huo, Yiwei Tony Zhu, and Yi-Jun Zhu

Subjects
*CANCER cells, *ESTROGEN receptors, *BREAST cancer research, *GENE amplification, *MOLECULAR biology
Abstract

ASH2L is a component of MLL complexes that confer H3K4 trimethylation. The ASH2L gene is located at 8q11-12, which is often amplified in breast cancers. We found that increased ASH2L expression, which can result from gene amplification, is often correlated with increased ERαexpression in both breast cancer cell lines and primary breast cancers. Forced expression of ASH2L induced ERα expression in mammary epithelial cells, whereas depletion of ASH2L suppressed ERα expression in breast cancer cells. To understand the mechanism by which ASH2L regulates ERα expression, we identified GATA3 as the binding protein of ASH2L. ASH2L was shown to potentiate the transcriptional activity of GATA3. ASH2L was recruited to the enhancer of the ERα gene through GATA3 to promote ERα transcription. This study established thatASH2L enhances ERα expression as a coactivator of GATA3 in breast cancers. [ABSTRACT FROM AUTHOR]

Published
2014
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4. Null Mutation of Peroxisome Proliferator-activated Receptor-interacting Protein in Mammary Glands Causes Defective Mammopoiesis.

Author

Chao Qi, Kashireddy, Papreddy, Yiwei Tony Zhu, Rao, Sambasiva M., and Yi-Jun Zhu

Subjects
*GENETIC mutation, *NUCLEAR receptors (Biochemistry), *PEROXISOMES, *MAMMARY glands, *ESTROGEN, *EPITHELIAL cells, *CELL proliferation -- Molecular aspects, *BIOCHEMISTRY
Abstract

To investigate the role of nuclear receptor coactivator peroxisome proliferator-activated receptor-interacting protein (PRIP) in mammary gland development, we generated a conditional null mutation of PRIP in mammary glands. In PRIP-deficient mammary glands, the elongation of ducts during puberty was not affected, but the numbers of ductal branches were decreased, a condition that persisted long after puberty, indicating that the potential of ductal branching was impaired. During pregnancy, PRIP-deficient mammary glands exhibited decreased alveolar density. The lactating PRIP-deficient glands contained scant lobuloalveoli with many adipocytes, whereas the wild type glands were composed of virtually no adipocytes but mostly lobuloalveoli. As a result, PRIP mammary-deficient glands could not produce enough milk to nurse all the pups during lactation. The ductal branching of mammary glands in response to estrogen treatment was attenuated in PRIP mutant glands. Whereas the proliferation index was similar between wild type and PRIP-deficient glands, increased apoptosis was observed in PRIP-deficient glands. PRIP-deficient glands expressed increased amphiregnlin, transforming growth factor-α, and betacellulin mRNA as compared with wild type glands. The differentiated function of PRIP-deficient mammary epithelial cells was largely intact, as evidenced by the expression of abundant β-casein, whey acidic protein (WAP), and WDNM1 mRNA. We conclude that PRIP is important for normal mammary gland development. [ABSTRACT FROM AUTHOR]

Published
2004
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