Transcriptomes of human prostate cells

Oudes, Asa; Campbell, Dave S; Sorensen, Carrie M.; Walashek, Laura S; True, Lawrence D.; Liu, Alvin Y.

doi:10.1186/1471-2164-7-92

Cited by 65 publications

(91 citation statements)

References 30 publications

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“…The majority of group C genes were indeed overexpressed in patient-derived luminal compared to basal cells (Oudes et al., 2006) (Figure 4A and S3), implying that another transcription factor, distinct from RA, may regulate group C to sustain and promote gene expression during luminal differentiation. Because systemic and niche-driven AR-mediated signaling is the main regulator of luminal differentiation in prostate and is capable of inducing luminal differentiation, even in 3D culture, with an obligatory contribution from stroma (Lang et al., 2006), we assessed the responsiveness of group C to AR stimulation in publically available microarray data.…”

Section: Resultsmentioning

confidence: 99%

Conserved Two-Step Regulatory Mechanism of Human Epithelial Differentiation

et al. 2014

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SummaryHuman epithelia are organized in a hierarchical structure, where stem cells generate terminally differentiated cells via intermediate progenitors. This two-step differentiation process is conserved in all tissues, but it is not known whether a common gene set contributes to its regulation. Here, we show that retinoic acid (RA) regulates early human prostate epithelial differentiation by activating a tightly coexpressed set of 80 genes (e.g., TMPRSS2). Response kinetics suggested that some of these genes could be direct RA targets, whereas others are probably responding indirectly to RA stimulation. Comparative bioinformatic analyses of published tissue-specific microarrays and a large-scale transcriptomic data set revealed that these 80 genes are not only RA responsive but also significantly coexpressed in many human cell systems. The same gene set preferentially responds to androgens during terminal prostate epithelial differentiation, implying a cell-type-dependent interplay between RA and tissue-specific transcription factor-mediated signaling in regulating the two steps of epithelial differentiation.

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Section: Resultsmentioning

confidence: 99%

Conserved Two-Step Regulatory Mechanism of Human Epithelial Differentiation

et al. 2014

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“…Differential gene expression analysis from array datasets was described in our previous publications [3, 44]. The obtained array CEL files were loaded into GeneSpring 7.2 (Agilent Technologies), which used an analysis algorithm of the open source Bioconductor project [45].…”

Section: Methodsmentioning

confidence: 99%

“…Small miRNA in vesicles are transported from producer cell to recipient cell to alter gene expression [2]. In benign prostate glands, three major cell types can be distinguished: CD26 + luminal secretory cells, CD104 + basal epithelial cells and CD49a + stromal cells [3]. In tumor glands only two major cell types are distinguished: CD26 + cancer epithelial cells and CD90 + cancer-associated stromal cells [4, 5].…”

Section: Introductionmentioning

confidence: 99%

Cancer-secreted AGR2 induces programmed cell death in normal cells

et al. 2016

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Anterior Gradient 2 (AGR2) is a protein expressed in many solid tumor types including prostate, pancreatic, breast and lung. AGR2 functions as a protein disulfide isomerase in the endoplasmic reticulum. However, AGR2 is secreted by cancer cells that overexpress this molecule. Secretion of AGR2 was also found in salamander limb regeneration. Due to its ubiquity, tumor secretion of AGR2 must serve an important role in cancer, yet its molecular function is largely unknown. This study examined the effect of cancer-secreted AGR2 on normal cells. Prostate stromal cells were cultured, and tissue digestion media containing AGR2 prepared from prostate primary cancer 10-076 CP and adenocarcinoma LuCaP 70CR xenograft were added. The control were tissue digestion media containing no AGR2 prepared from benign prostate 10-076 NP and small cell carcinoma LuCaP 145.1 xenograft. In the presence of tumor-secreted AGR2, the stromal cells were found to undergo programmed cell death (PCD) characterized by formation of cellular blebs, cell shrinkage, and DNA fragmentation as seen when the stromal cells were UV irradiated or treated by a pro-apoptotic drug. PCD could be prevented with the addition of the monoclonal AGR2-neutralizing antibody P3A5. DNA microarray analysis of LuCaP 70CR media-treated vs. LuCaP 145.1 media-treated cells showed downregulation of the gene SAT1 as a major change in cells exposed to AGR2. RT-PCR analysis confirmed the array result. SAT1 encodes spermidine/spermine N1-acetyltransferase, which maintains intracellular polyamine levels. Abnormal polyamine metabolism as a result of altered SAT1 activity has an adverse effect on cells through the induction of PCD.

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“…Additionally, immunoelectron microscopic analysis with autoantibodies that recognize several centromeric proteins revealed that each pre-kinetochore complex forms a stable, but highly dynamic association with the filaments of the nuclear matrix, proposing that the strikingly mobile properties of the centromeric complex may be facilitated by anchoring to the matrix network (39). Historically, alterations in the composition, number, size, and intranuclear localization of nucleoli were used as an early indication of cancer and to distinguish a few types of tumor cells from normal cells (40,41). Alterations in the nuclear matrix composition are also known to be cell type-and tumor-specific and have been used for the development of protein biomarkers of cancer (42).…”

Section: Discussionmentioning

confidence: 99%

New Centromeric Component CENP-W Is an RNA-associated Nuclear Matrix Protein That Interacts with Nucleophosmin/B23 Protein

Chun¹,

Park²,

Koh

et al. 2011

Journal of Biological Chemistry

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CENP-W was originally identified as a putative oncogene, cancer-upregulated gene 2 (CUG2) that was commonly up-regulated in many cancer tissues. Recently, CENP-W has also been identified as a new centromeric component that interacts with CENP-T. As a complex with CENP-T, CENP-W plays crucial roles in assembly of the functional kinetochore complex. In this study, the subnuclear localization of CENP-W was extensively analyzed using various approaches. We found that ectopically expressed CENP-W primarily accumulated in the nucleolus and remained substantially associated with the nucleolus in stable cells. The following fractionation study also showed that CENP-W is associated with RNA as well as DNA. Moreover, a considerable amount of CENP-W was found in the nuclear mesh-like structure, nuclear matrix, possibly indicating that CENP-W participates in diverse subnuclear activities. Finally, biochemical affinity binding analysis revealed that CENP-W specifically interacts with the nucleolar phosphoprotein, nucleophosmin (B23). Depletion of cellular B23 by siRNA treatment induced a dramatic decrease of CENP-W stability and severe mislocalization during prophase. Our data proposed that B23 may function in the assembly of the kinetochore complex by interacting with CENP-W during interphase.

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Transcriptomes of human prostate cells

Cited by 65 publications

References 30 publications

Conserved Two-Step Regulatory Mechanism of Human Epithelial Differentiation

Conserved Two-Step Regulatory Mechanism of Human Epithelial Differentiation

Cancer-secreted AGR2 induces programmed cell death in normal cells

New Centromeric Component CENP-W Is an RNA-associated Nuclear Matrix Protein That Interacts with Nucleophosmin/B23 Protein

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