The combined immunodetection of AP-2α and YY1 transcription factors is associated with ERBB2 gene overexpression in primary breast tumors

Allouche, Abdelkader; Nolens, Grégory; Tancredi, Annalisa; Delacroix, Laurence; Mardaga, Julie; Fridman, Viviana; Winkler, Rosita; Boniver, Jacques; Delvenne, Philippe; Begon, Dominique

doi:10.1186/bcr1851

Cited by 97 publications

(98 citation statements)

References 30 publications

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“…The putative role of YY1 in tumorigenesis is supported by its known interaction in the cell cycle regulation 4 and, accordingly, many studies were conducted to evaluate the involvement of YY1 in several solid tumor types. [14][15][16][17][18][19] In this study we have provided evidence that YY1 is expressed at significantly higher levels in high-grade lymphomas, including Burkitt's Lymphoma and DLBCL, when compared to normal B cells. DLBCL is the most frequent non-Hodgkin's lymphoma subtype, accounting for 30% to 35% of all lymphoma cases.…”

Section: Discussionmentioning

confidence: 82%

Yin Yang 1 overexpression in diffuse large B-cell lymphoma is associated with B-cell transformation and tumor progression

Castellano¹,

Torrisi²,

Ligresti³

et al. 2010

Cell Cycle

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Section: Discussionmentioning

confidence: 82%

Yin Yang 1 overexpression in diffuse large B-cell lymphoma is associated with B-cell transformation and tumor progression

Castellano¹,

Torrisi²,

Ligresti³

et al. 2010

Cell Cycle

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“…Transcription factors such as AP-2 (8), YY1 (20), ETS (21), YB-1 (22), and EGR2 (23) have been shown to be recruited to the promoter of ERBB2 and play a role in its overexpression in breast cancer cells. Therefore, understanding the mechanisms governing the repressive and positive regulation of ERBB2 expression and its neighboring genes in the amplified locus is of considerable importance in identifying the transcription factors and molecular events involved in the establishment of ERBB2-positive tumors.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional Control of the ERBB2 Amplicon by ERRα and PGC-1β Promotes Mammary Gland Tumorigenesis

et al. 2010

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Overexpression of ERBB2 and its neighboring genes on chromosome 17 occurs in approximately 25% of breast tumors and is associated with poor prognosis. While amplification of the 17q12-21 chromosomal region often correlates with an increase in the transcriptional rates of the locus, the molecular mechanisms and the factors involved in the coordinated expression of genes residing within the ERBB2 amplicon remain largely unknown. Here we demonstrate that estrogen-related receptor a (ERRa, NR3B1) and its coregulator PGC-1b are key effectors in this process. Using a mouse model of ERBB2-initiated mammary tumorigenesis, we first show that ablation of ERRa significantly delays ERBB2-induced tumor development and lowers the levels of amplicon transcripts. Chromosome 17q-wide binding site location analyses in human breast cancer cells show preferential recruitment of ERRa to DNA segments associated with the ERBB2 amplicon. Furthermore, ERRa directs the corecruitment of the coactivator PGC-1b to segments in the 17q12 region and the recruitment of RNA polymerase II to the promoters of the ERBB2 and coamplified genes. ERRa and PGC-1b also participate in the de-repression of ERBB2 expression through competitive genomic cross-talk with estrogen receptor a (ERa) and, as a consequence, influence tamoxifen sensitivity in breast cancer cells. Taken together, our results suggest that ERRa and PGC-1b are key players in the etiology of malignant breast cancer by coordinating the transcriptional regulation of genes located in the 17q12 region, a process that also involves interference with the repressive function of ERa on ERBB2 expression.

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“…Girdin has been reported to be highly expressed in invasive colon and breast carcinoma tissues, and high levels of Girdin expression correlate significantly with ErbB2 oncogene expression in breast cancer (Garcia-Marcos et al, 2011;Jiang et al, 2008;Ling et al, 2011). Interestingly, ErbB2 expression is also transcriptionally regulated by AP-2α and is associated with AP-2α in breast cancer (Allouche et al, 2008;Bosher et al, 1995;Pellikainen et al, 2004). Therefore, it is possible that accumulated genetic and epigenetic mutations during cancer progression might deregulate PAR-3, leading to aberrant transcriptional activity and/or increased expression of AP-2α, and resulting in Girdin and ErbB2 overexpression.…”

Section: Biological Implications Of the Par-3-ap-2-girdin Pathway Inmentioning

confidence: 90%

Regulation of epithelial cell polarity by PAR-3 depends on Girdin transcription and Girdin–Gαi3 signaling

Sasaki

Kakuwa

Akimoto

et al. 2015

Journal of Cell Science

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Epithelial apicobasal polarity has fundamental roles in epithelial physiology and morphogenesis. The PAR complex, comprising PAR-3, PAR-6 and aPKC, is involved in determining cell polarity in various biological contexts, including in epithelial cells. However, it is not fully understood how the PAR complex induces apicobasal polarity. In this study, we show that PAR-3 regulates the protein expression of Girdin (GIV/CCDC88A), a guanine nucleotide exchange factor (GEF) for heterotrimeric Gαi subunits, at the transcriptional level by cooperating with the AP-2 transcription factor. In addition, we confirmed that PAR-3 physically interacts with Girdin, and show that Girdin, together with the Gαi3, controls tight junction formation, apical domain development and actin organization downstream of PAR-3. Taken together, our findings suggest that transcriptional upregulation of Girdin and Girdin–Gαi3 signaling play crucial roles in regulating epithelial apicobasal polarity via the PAR complex.

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The combined immunodetection of AP-2α and YY1 transcription factors is associated with ERBB2 gene overexpression in primary breast tumors

Cited by 97 publications

References 30 publications

Yin Yang 1 overexpression in diffuse large B-cell lymphoma is associated with B-cell transformation and tumor progression

Yin Yang 1 overexpression in diffuse large B-cell lymphoma is associated with B-cell transformation and tumor progression

Transcriptional Control of the ERBB2 Amplicon by ERRα and PGC-1β Promotes Mammary Gland Tumorigenesis

Regulation of epithelial cell polarity by PAR-3 depends on Girdin transcription and Girdin–Gαi3 signaling

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