Human MageB2 Protein Expression Enhances E2F Transcriptional Activity, Cell Proliferation, and Resistance to Ribotoxic Stress

Peche, Leticia Y.; Ladelfa, María Fátima; Toledo, María Fernanda; Mano, Miguel; Laiseca, Julieta Eva; Schneider, Claudio; Monte, Martín

doi:10.1074/jbc.m115.671982

Cited by 25 publications

(19 citation statements)

References 54 publications

(54 reference statements)

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“…Among the 38 genes exclusively expressed in SKOV-3 cells (Supplementary Table S2), ALDH1A1 [26], GABRA3 [27], FOLR1 [28], DPYSL5 [29], CGB8 [30], C8orf4 [31] and MAGEB2 [32] could be intriguing for the development and maintenance of the neoplastic phenotype. Similarly, among the 82 genes expressed only in FT194 cells (Supplementary Table S2) CDKN2A [33], MT1G [34], GPX7 [35], HCK [36], ZBTB16 [37] could be looked at as interesting genes being tumor suppressor epigenetically silenced in cancer cells.…”

Section: Resultsmentioning

confidence: 99%

Candidate genes and pathways downstream of PAX8 involved in ovarian high-grade serous carcinoma

et al. 2016

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Understanding the biology and molecular pathogenesis of ovarian epithelial cancer (EOC) is key to developing improved diagnostic and prognostic indicators and effective therapies. Although research has traditionally focused on the hypothesis that high-grade serous carcinoma (HGSC) arises from the ovarian surface epithelium (OSE), recent studies suggest that additional sites of origin exist and a substantial proportion of cases may arise from precursor lesions located in the Fallopian tubal epithelium (FTE). In FTE cells, the transcription factor PAX8 is a marker of the secretory cell lineage and its expression is retained in 96% of EOC. We have recently reported that PAX8 is involved in the tumorigenic phenotype of ovarian cancer cells. In this study, to uncover genes and pathways downstream of PAX8 involved in ovarian carcinoma we have determined the molecular profiles of ovarian cancer cells and in parallel of Fallopian tube epithelial cells by means of a silencing approach followed by an RNA-seq analysis. Interestingly, we highlighted the involvement of pathways like WNT signaling, epithelial-mesenchymal transition, p53 and apoptosis. We believe that our analysis has led to the identification of candidate genes and pathways regulated by PAX8 that could be additional targets for the therapy of ovarian carcinoma.

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Section: Resultsmentioning

confidence: 99%

Candidate genes and pathways downstream of PAX8 involved in ovarian high-grade serous carcinoma

et al. 2016

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“…Recent work by Peche et al also showed that MAGE-B2 interacts with HDAC1, an E2F1 repressor, to enhance E2F1 transactivation [60]. Therefore, whereas some type II MAGEs target and inhibit E2F function, other type I MAGEs may stimulate E2F activity to promote tumor cell proliferation.…”

Section: Function and Mechansim Of Mage-ring Ligasesmentioning

confidence: 99%

“…For example, knockdown of mouse Mage-b genes reduces cell viability in melanoma and mast cell lines [37, 155]. Similarly, MAGE-B2 promotes cell proliferation in transformed oral keratinocytes, osteosarcoma, and colon cancer cell lines [60, 151]. Moreover, Mage-b knockdown suppresses growth in a syngeneic mouse model, whereas over-expression of MAGE-B2 enhances tumor growth in mice [37, 60].…”

Section: Mages In Diseasementioning

confidence: 99%

“…Similarly, MAGE-B2 promotes cell proliferation in transformed oral keratinocytes, osteosarcoma, and colon cancer cell lines [60, 151]. Moreover, Mage-b knockdown suppresses growth in a syngeneic mouse model, whereas over-expression of MAGE-B2 enhances tumor growth in mice [37, 60]. Likewise, MAGE-C2 has also been shown to promote cell proliferation in malignant melanoma cells and tumor metastasis in vivo by enhancing STAT3 signaling [52, 156].…”

Section: Mages In Diseasementioning

confidence: 99%

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A Comprehensive Guide to the MAGE Family of Ubiquitin Ligases

Lee

Potts

2017

Journal of Molecular Biology

107

118

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Melanoma antigen (MAGE) genes are conserved in all eukaryotes and encode for proteins sharing a common MAGE homology domain. Although only a single MAGE gene exists in lower eukaryotes, the MAGE family rapidly expanded in eutherians and consists of more than 50 highly conserved genes in humans. A subset of MAGEs initially garnered interest as cancer biomarkers and immunotherapeutic targets due to their antigenic properties and unique expression pattern that is primary restricted to germ cells and aberrantly re-activated in various cancers. However, further investigation revealed that MAGEs not only drive tumorigenesis, but also regulate pathways essential for diverse cellular and developmental processes. Therefore, MAGEs are implicated in a broad range of diseases including neurodevelopmental, renal, and lung disorders, as well as cancer. Recent biochemical and biophysical studies indicate that MAGEs assemble with E3 RING ubiquitin ligases to form MAGE-RING ligases (MRLs) and act as regulators of ubiquitination by modulating ligase activity, substrate specification, and subcellular localization. Here, we present a comprehensive guide to MAGEs highlighting the molecular mechanisms of MRLs, their physiological roles in germ cell and neural development, oncogenic functions in cancer, and potential as therapeutic targets in disease.

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“…For example, BORIS/CTCFL up-regulates h-TERT (62), and through poorly defined mechanisms inhibits apoptosis in cancer cells (63). MAGE-A11 inhibits function of the RBL1/ p107 tumor suppressor (64), and MAGE-B2 enhances E2F activity to promote cell cycle progression (65). MAGE-A2, and MAGE-C2 impair p53 function by directly inhibiting binding of p53 to target promoters, promoting deacetylation (inactivation) of p53, or by enhancing ubiquitin-mediated degradation of this tumor suppressor (66-68).…”

Section: Loss Of Imprinting (Loi) and De-repression Of Cg Genesmentioning

confidence: 99%