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This work was supported by:Fondo de Investigacion Sanitaria, ISCIII, grant number PI20-194, co-funded by ERDF/ESF, "Investing in your future".Generalitat Valenciana grant BEFPI/2013/060 for BPB.Generalitat Valenciana grant APOST 2016/001 for BPB.FEBS Short-Term Fellowship 2014 for BPB.Ministerio de Educacion, Cultura y Deporte grant FPU13/02755 for JMPS.Asociacion Espanola contra el cancer, AECC predoctoral grant for AMF.Part of the equipment employed in this work has been funded by Generalitat Valenciana and co-financed with ERDF funds (OP ERDF of Comunitat Valenciana 2014-2020).
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Martinez-Ferriz, ArantxaAuthorNew roles for AP-1/JUNB in cell cycle control and tumorigenic cell invasion via regulation of cyclin E1 and TGF-β2
Publicated to:Genome Biology. 23 (1): 252- - 2022-12-09 23(1), DOI: 10.1186/s13059-022-02800-0
Authors: Perez-Benavente, Beatriz; Fathinajafabadi, Alihamze; de la Fuente, Lorena; Gandia, Carolina; Martinez-Ferriz, Arantxa; Pardo-Sanchez, Jose Miguel; Milian, Lara; Conesa, Ana; Romero, Octavio A; Carretero, Julian; Matthiesen, Rune; Jariel-Encontre, Isabelle; Piechaczyk, Marc; Farras, Rosa
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Abstract
Background: JUNB transcription factor contributes to the formation of the ubiquitous transcriptional complex AP-1 involved in the control of many physiological and disease-associated functions. The roles of JUNB in the control of cell division and tumorigenic processes are acknowledged but still unclear. Results: Here, we report the results of combined transcriptomic, genomic, and functional studies showing that JUNB promotes cell cycle progression via induction of cyclin El and repression of transforming growth factor (TGF)-beta 2 genes. We also show that high levels ofJUNB switch the response of TGF-beta 2 stimulation from an antiproliferative to a pro-invasive one, induce endogenous TGF-beta 2 production by promoting TGF-beta 2 mRNA translation, and enhance tumor growth and metastasis in mice. Moreover, tumor genomic data indicate that JUNB amplification associates with poor prognosis in breast and ovarian cancer patients. Conclusions: Our results reveal novel functions for JUNB in cell proliferation and tumor aggressiveness through regulation of cyclin E1 and TGF-beta 2 expression, which might be exploited for cancer prognosis and therapy.
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Bibliometric impact. Analysis of the contribution and dissemination channel
The work has been published in the journal Genome Biology due to its progression and the good impact it has achieved in recent years, according to the agency WoS (JCR), it has become a reference in its field. In the year of publication of the work, 2022, it was in position 5/171, thus managing to position itself as a Q1 (Primer Cuartil), in the category Genetics & Heredity. Notably, the journal is positioned above the 90th percentile.
From a relative perspective, and based on the normalized impact indicator calculated from World Citations provided by WoS (ESI, Clarivate), it yields a value for the citation normalization relative to the expected citation rate of: 2.07. This indicates that, compared to works in the same discipline and in the same year of publication, it ranks as a work cited above average. (source consulted: ESI Nov 14, 2024)
This information is reinforced by other indicators of the same type, which, although dynamic over time and dependent on the set of average global citations at the time of their calculation, consistently position the work at some point among the top 50% most cited in its field:
- Field Citation Ratio (FCR) from Dimensions: 11.86 (source consulted: Dimensions Jul 2025)
Specifically, and according to different indexing agencies, this work has accumulated citations as of 2025-07-27, the following number of citations:
- WoS: 22
- Europe PMC: 28
Impact and social visibility
Leadership analysis of institutional authors
This work has been carried out with international collaboration, specifically with researchers from: France; Portugal; United States of America.