PIAS1 Promotes Lymphomagenesis through MYC Upregulation

Rabellino, Andrea; Melegari, Margherita; Tompkins, Van S.; Chen, Weina; Ness, Brian G. Van; Teruya‐Feldstein, Julie; Conacci‐Sorrell, Maralice; Janz, Siegfried; Scaglioni, Pier Paolo

doi:10.1016/j.celrep.2016.05.015

Cited by 38 publications

(52 citation statements)

References 51 publications

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“…SUMOylation not only prolongs MYC half-life preventing its proteasomal degradation, but also positively regulates MYC transcriptional activity. Significantly, we also demonstrated that MYC is SUMOylated in primary B-cell lymphomas (43). Furthermore, PIAS1-mediated SUMOylation is required to maintain the oncogenic activity of MYC in lymphoma cells.…”

Section: Pias1 Myc and Lymphomagenesissupporting

confidence: 61%

“…Recently, PIAS1 has been reported to account for MYC SUMOylation (43,44) (Fig.2D). K51/52 are the major MYC SUMOylation sites.…”

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 89%

“…In this regards, it is noteworthy that PIAS1 is required also for the viability of MYC-dependent breast cancer and of lung cancer cells (43) (and AR unpublished results). These findings support the conclusion that PIAS1 is a requirement of other MYC-driven malignances.…”

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 92%

“…Furthermore, PIAS1-mediated SUMOylation is required to maintain the oncogenic activity of MYC in lymphoma cells. Accordingly, we found that PIAS1 and MYC are often co-expressed in human and murine diffuse large B-cell lymphoma (DLBCL) (43). This study also suggests that PIAS1 regulates MYC during B-cell maturation and activation in vitro .…”

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 99%

“…Instead, in conditions of up-regulation of MYC, as it often occurs in cancer, PIAS1 promotes the supra-physiological activation of MYC, contributing not only to B-cell lymphomagenesis but also to other cancer types (43). …”

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 99%

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The Role of PIAS SUMO E3-Ligases in Cancer

2017

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SUMOylation modifies the interactome, localization, activity and lifespan of its target proteins. This process regulates several cellular machineries, including transcription, DNA damage repair, cell-cycle progression and apoptosis. Accordingly, SUMOylation is critical in maintaining cellular homeostasis and its deregulation leads to the corruption of a plethora of cellular processes that contribute to disease states. Among the proteins involved in SUMOylation, the Protein Inhibitor of Activated STAT (PIAS) E3-ligases were initially described as transcriptional co-regulators. Recent findings also indicate that they have a role in regulating protein stability and signaling transduction pathways. PIAS proteins interact with up to 60 cellular partners affecting several cellular processes, most notably immune regulation and DNA repair, but also cellular proliferation and survival. Here we summarize the current knowledge about their role in tumorigenesis and cancer-related processes.

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Section: Pias1 Myc and Lymphomagenesissupporting

confidence: 61%

“…Recently, PIAS1 has been reported to account for MYC SUMOylation (43,44) (Fig.2D). K51/52 are the major MYC SUMOylation sites.…”

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 89%

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 92%

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 99%

Section: Pias1 Myc and Lymphomagenesismentioning

confidence: 99%

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The Role of PIAS SUMO E3-Ligases in Cancer

2017

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Regulation and Function of the MYC Oncogene

Kalkat

Resetca

Penn

2018

Encyclopedia of Life Sciences

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Regulation and Function of the MYC Oncogene

Kalkat¹,

Resetca²,

Penn³

2019

Encyclopedia of Life Sciences

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One of the most acclaimed features of the MYC oncogene family ( MYC, MYCL1 and MYCN ) is their prolific deregulation in cancer, which is often associated with poor prognosis and refractory disease. Multiple mechanisms can deregulate their expression in cancer, including chromosomal translocation, enhanced messenger ribonucleic acid (mRNA) and protein stability, gene amplification or enhancer hijacking. This MYC family of nuclear transcription factors regulates the expression of a multitude of target genes to control many critically important fundamental biological processes, including cellular proliferation, metabolism, apoptosis and embryonic development. MYC proteins are highly regulated, and many factors have been reported to control stability and activity via post‐translational modifications (PTMs). Decades of research into this potent oncogene family have revealed that while directly inhibiting MYC proteins in cancer remains challenging, there are multiple strategies to indirectly inhibit MYC in cancer. Developing such inhibitors to target MYC would have profound impact on patient care and outcome. Key Concepts The MYC family of oncogenes, composed of MYC, MYCN and MYCL1 , encode nuclear basic helix‐loop‐helix transcription factors. MYC family proteins contain highly conserved regions termed MYC boxes. MYC regulates many transcriptional targets and can have wide‐reaching effects on the epigenome and total cellular RNA content. MYC is essential for cellular proliferation and is a potent oncogene when it is deregulated in cancer. Deregulated, often elevated, MYC levels have been shown to drive tumourigenesis in many in vivo models. MYC activity and stability is regulated by post‐translational modifications, including phosphorylation, ubiquitylation, SUMOylation and acetylation.

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PIAS1 Promotes Lymphomagenesis through MYC Upregulation

Cited by 38 publications

References 51 publications

The Role of PIAS SUMO E3-Ligases in Cancer

The Role of PIAS SUMO E3-Ligases in Cancer

Regulation and Function of the MYC Oncogene

Regulation and Function of the MYC Oncogene

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