The Ets Factors PU.1 and Spi-B Regulate the Transcriptionin Vivo of P2Y10, a Lymphoid Restricted Heptahelical Receptor

Rao, Sridhar; Garrett‐Sinha, Lee Ann; Yoon, Jaesik; Simon, M. Celeste

doi:10.1074/jbc.274.48.34245

Cited by 40 publications

(34 citation statements)

References 65 publications

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“…Spi-B is first identified as a transcriptional activator, directly activating c-Rel (29), P2Y10 (30), and p50 (31). Our results show that Spi-B can also act as a transcriptional repressor.…”

Section: Discussionmentioning

confidence: 55%

Spi-B–Mediated Silencing of Claudin-2 Promotes Early Dissemination of Lung Cancer Cells from Primary Tumors

Niu

et al. 2017

Cancer Research

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Dissociation from epithelial sheets and invasion through the surrounding stroma are critical early events during epithelial cancer metastasis. Here we find that a lymphocyte lineage-restricted transcription factor, Spi-B, is frequently expressed in human lung cancer tissues. The Spi-B-expressing cancer cells coexpressed vimentin but repressed E-cadherin and exhibited invasive behavior. Increased Spi-B expression was associated with tumor grade, lymphatic metastasis, and short overall survival. Mechanistically, Spi-B disrupted intercellular junctions and enhanced invasiveness by reconfiguring the chromatin structure of the tight junction gene claudin-2 (CLDN2) and repressing its transcription. These data suggest that Spi-B participates in mesenchymal invasion, linking epithelial cancer metastasis with a lymphatic transcriptional program.

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Section: Discussionmentioning

confidence: 55%

Spi-B–Mediated Silencing of Claudin-2 Promotes Early Dissemination of Lung Cancer Cells from Primary Tumors

Niu

et al. 2017

Cancer Research

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“…Weak BCR signaling combined with signaling through the Notch pathway reinforces the MZ B cell fate (13). BCR signaling was previously shown to be impaired in PUB mice (20), and PU.1 and Spi-B were subsequently shown to regulate several genes involved in modulation of BCR signaling (48,49). BCR signaling is also modulated by ectopic expression of Spi-C in B cells (24).…”

Section: Discussionmentioning

confidence: 99%

Regulation of Follicular B Cell Differentiation by the Related E26 Transformation-Specific Transcription Factors PU.1, Spi-B, and Spi-C

DeKoter

Geadah

Khoosal

et al. 2010

The Journal of Immunology

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“…Both PU.1 and Spi-B are expressed in the B cell lineage beginning at the pro-B cell stage and appear to interact with identical DNA binding sites (15). Therefore in developing B cells, the available evidence indicates that PU.1 and Spi-B are functionally interchangeable (22,23).…”

Section: Cells (4)mentioning

confidence: 99%

Analysis of Gene Expression and Ig Transcription in PU.1/Spi-B-Deficient Progenitor B Cell Lines

Schweitzer

DeKoter

2004

The Journal of Immunology

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A number of presumptive target genes for the Ets-family transcription factor PU.1 have been identified in the B cell lineage. However, the precise function of PU.1 in B cells has not been studied because targeted null mutation of the PU.1 gene results in a block to lymphomyeloid development at an early developmental stage. In this study, we take advantage of recently developed PU.1−/−Spi-B−/− IL-7 and stromal cell-dependent progenitor B (pro-B) cell lines to analyze the function of PU.1 and Spi-B in B cell development. We show that contrary to previously published expectations, PU.1 and/or Spi-B are not required for Ig H chain (IgH) gene transcription in pro-B cells. In fact, PU.1−/−Spi-B−/− pro-B cells have increased levels of IgH transcription compared with wild-type pro-B cells. In addition, high levels of Igκ transcription are induced after IL-7 withdrawal of wild-type or PU.1−/−Spi-B−/− pro-B cells. In contrast, we found that Igλ transcription is reduced in PU.1−/−Spi-B−/− pro-B cells relative to wild-type pro-B cells after IL-7 withdrawal. These results suggest that Igλ, but not IgH or Igκ, transcription, is dependent on PU.1 and/or Spi-B. The PU.1−/−Spi-B−/− pro-B cells have other phenotypic changes relative to wild-type pro-B cells including increased proliferation, increased CD25 expression, decreased c-Kit expression, and decreased RAG-1 expression. Taken together, our observations suggest that reduction of PU.1 and/or Spi-B activity in pro-B cells promotes their differentiation to a stage intermediate between late pro-B cells and large pre-B cells.

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The Ets Factors PU.1 and Spi-B Regulate the Transcriptionin Vivo of P2Y10, a Lymphoid Restricted Heptahelical Receptor

Abstract: To investigate the in vivo functions of PU.1 and Spi-B, two highly related Ets transcription factors, we previously generated PU.

Cited by 40 publications

References 65 publications

Spi-B–Mediated Silencing of Claudin-2 Promotes Early Dissemination of Lung Cancer Cells from Primary Tumors

Spi-B–Mediated Silencing of Claudin-2 Promotes Early Dissemination of Lung Cancer Cells from Primary Tumors

Regulation of Follicular B Cell Differentiation by the Related E26 Transformation-Specific Transcription Factors PU.1, Spi-B, and Spi-C

Analysis of Gene Expression and Ig Transcription in PU.1/Spi-B-Deficient Progenitor B Cell Lines

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