Study of MDM2 and SUMO-1 expression in actinic cheilitis and lip cancer

Alves, Mônica Ghislaine Oliveira; Delgado, Adriana da Mota; Balducci, Ivan; Carvalho, Yasmin Rodarte; Cavalcante, Ana Sueli Rodrigues; Almeida, Janete Días

doi:10.1007/s00403-014-1500-8

Cited by 11 publications

(10 citation statements)

References 22 publications

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“…Indeed, SUMO1 and SUMO2/3 levels were higher in low-grade astrocytoma and even more in glioblastoma multiforme brain tumors, which carry a very poor prognosis [60]. Consistently, SUMO1 overexpression was detected in hepatocellular carcinoma patients [97], and in lip cancer [98] suggesting that the expression level of SUMO1 may aid their diagnosis. Moreover, SUMO1 was expressed at much higher levels in oral squamous cell carcinoma tissue than normal oral epithelium, and patients with SUMO1 and Mdm2 overexpression experienced more frequently local recurrences after initial treatments [99].…”

Section: Sumo Proteinsmentioning

confidence: 63%

“…Oral squamous cell carcinoma Diagnosis [92] Breast Prognosis [93] SENP6 Breast Diagnosis [94] SENP7 Breast Diagnosis [95] USPL1 Breast Risk assessment [96] SUMO1, SUMO2/3 Astrocytic brain Diagnosis, progression [60] SUMO1 Hepatocellular carcinoma Diagnosis [97] Lip Diagnosis [98] Oral squamous cell carcinoma Diagnosis, prognosis [99] AML: Acute myeloid leukemia; MDS: Myelodysplastic syndrome.…”

Section: Senp5mentioning

confidence: 99%

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SUMO pathway components as possible cancer biomarkers

Mattoscio

Chiocca

2015

Future Oncol.

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SUMOylation is a key post-translational modification that regulates crucial cellular functions and pathological processes. Recently, Small Ubiquitin-related MOdifier (SUMO) modification has emerged as a fundamental route that may drive different steps of human tumorigenesis. Indeed, alteration in expression or activity of one of the different SUMO pathway components may completely subvert cellular properties through fine-tuning modulation of protein(s) involved in carcinogenic pathways, leading to altered cell proliferation, apoptosis resistance and metastatic potential. Here we describe some of the most interesting findings pointing to a clear link between SUMO pathway and human malignancies. Importantly, a putative role for SUMO enzymes to predict cancer behavior can be speculated, and thus the possible application of alterations in SUMO pathway components as tumor biomarkers is discussed.

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Section: Sumo Proteinsmentioning

confidence: 63%

Section: Senp5mentioning

confidence: 99%

SUMO pathway components as possible cancer biomarkers

Mattoscio

Chiocca

2015

Future Oncol.

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“…SUMOylation via PIAS1 promotes ubiquitylation via the Stubl RNF4 and subsequent proteasomal degradation, thereby reducing transcriptional activity [73]. liver Overexpression of SUMO1 [111] colon Overexpression of SUMO1 [112] lip Overexpression of SUMO1 [113] gastric Upregulation of SUMO1 pseudogene3 [114] SUMO activating enzyme SAE1/2 gastric Overexpression of SAE2 [115] lung Overexpression of SAE2 [116] breast Low expression of SAE1 and SAE2 correlates with better survival [69] SUMO conjugating enzyme UBC9 lung Overexpression of UBC9 [117] primary colon and primary prostate Overexpression of UBC9 [64] metastatic breast, prostate and lung Downregulation of UBC9 [64] breast High levels of UBC9 correlate with higher risk for cancer and poor response to chemotherapy [118,119] multiple myeloma Overexpression of UBC9 [120] ovaries Overexpression of UBC9 [63] brain Overexpression of UBC9 [121] SUMO ligases PIAS1, PIAS2, PIAS3, PIASγ…”

Section: Figure 2 Sumoylation Of Important Cell Cycle Regulatorsmentioning

confidence: 99%

SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer

Eifler

Vertegaal

2015

Trends in Biochemical Sciences

232

201

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SUMOylation plays critical roles during cell cycle progression. Many important cell cycle regulators, including many oncogenes and tumor suppressors, are functionally regulated via SUMOylation. The dynamic SUMOylation pattern observed throughout the cell cycle is ensured via distinct spatial and temporal regulation of the SUMO machinery. Additionally, SUMOylation cooperates with other post-translational modifications to mediate cell cycle progression. Deregulation of these SUMOylation and deSUMOylation enzymes causes severe defects in cell proliferation and genome stability. Different types of cancers were recently shown to be dependent on a functioning SUMOylation system, a finding that could potentially be exploited in anti-cancer therapies. KeywordsSUMO; mitosis; SUMOylation; cancer; cell cycle SUMO: a ubiquitin-like modifier that regulates nuclear processesThe complexity of eukaryotic proteomes is widely expanded by protein processing and a vast array of posttranslational modifications. The quick and reversible attachment of small modifiers is essential for all cellular processes and ensures dynamic and rapid responses to extracellular and intracellular stimuli. Apart from chemical modifications such as phosphorylation [1], glycosylation [2] and acetylation [3], small polypeptides can be attached to proteins, resulting in a change in the activity, localization, half-life or interactome of the target protein. Since the initial discovery of ubiquitin, the founding member of these small protein posttranslational modifications in 1975 [4], a large family of structurally related ubiquitin-like modifiers has been uncovered including SUMO, Nedd8, ISG15, FAT10, FUB1, UFM1, URM1, Atg12 and Atg8 [5][6][7][8]. The attachment of these small ubiquitin-like modifiers is catalysed by an enzymatic cascade consisting of an activating enzyme (E1), a conjugating enzyme (E2) and a ligase (E3), and can be reversed by specific and cell cycle control. It is therefore not surprising that SUMO signal transduction has been implicated in the development of several different cancer types, which could potentially be exploited in anti-cancer therapies. In this review we will focus on the role of SUMO in cell cycle regulation, specifically highlighting its physiological relevance and its deregulation in cancer. Recent progress includes the identification of many novel SUMO substrates with important roles in cell cycle progression using proteomic approaches, and the demonstration that different mouse cancer models are dependent on a functioning SUMOylation system. Switching of SUMOylation in these cancer models caused a proliferation block of the cancer cells, showing that SUMO conjugating enzymes are potential drug targets. Europe PMC Funders Group Twenty years of SUMO research in cell cycle controlSUMO was linked to cell cycle progression even before the identification of the small protein modifier itself. Twenty years ago, the yeast SUMO conjugating enzyme Ubc9 was first proposed to be a ubiquitin conjugating enzyme. Ubc9 was s...

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“…Actinic cheilitis (AC) is a potentially malignant disorder of the lip caused by chronic and excessive exposure to ultraviolet (UV) radiation . The prevalence of AC can range from 11.4% to 39.6% in populations chronically exposed to UV radiation, such as fishermen and rural and construction workers, and transformation to squamous cell carcinoma (SCC) is observed in 16.9% to 20.0% of cases . Although the understanding of this process has grown in recent years, the molecular events involved in lip carcinogenesis are not fully elucidated.…”

Section: Introductionmentioning

confidence: 99%