SUMO-specific protease 1 regulates the in vitro and in vivo growth of colon cancer cells with the upregulated expression of CDK inhibitors

Xu, Ying; Li, Jie; Zuo, Yongchun; Deng, Jiong; Wang, Li‐Shun; Chen, Guoqiang

doi:10.1016/j.canlet.2011.05.019

Cited by 76 publications

(62 citation statements)

References 28 publications

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“…Whether it represents a common modification downstream from other anti-mitogenic signals able to stabilize nuclear p27, such as serum deprivation or contact inhibition, will be the matter of future investigations. In accord with our present observations, it has been reported that inhibition of SUMO-specific protease 1 (SENP1) results in increased p27 levels in colon cancer (Xu et al, 2011), corroborating the possibility that the pathway described here represents a common mechanism of p27 regulation. Our bioinformatic analyses revealed that p27 could be SUMOylated on many different lysines, even if none of the 13 lysine residues lies within the classical SUMO consensus sequence (CKxE/D) (Anckar and Sistonen, 2007), a possibility already for 3 h. Vinculin was used as loading control and phosphorylated Smad2 (pSer 465/467) was used as a marker of TGFb signaling activation.…”

Section: Discussionsupporting

confidence: 82%

SUMOylation regulates p27^Kip1stability and localization in response to TGFβ

et al. 2015

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Section: Discussionsupporting

confidence: 82%

SUMOylation regulates p27^Kip1stability and localization in response to TGFβ

et al. 2015

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“…The family of sentrin/SUMO-specific proteases (SENPs) is one of a group of enzymes that process newly synthesized SUMO1s into the conjugate form and catalyze the deconjugation of SUMO-containing species to regulate the function of the SUMO protein. SENP1, a member of the SENP family, has been reported to be overexpressed in colon cancer tissues (5) and has been demonstrated to regulate androgen receptor transactivation by targeting histone deacetylase I, and induce c-Jun activity through de-SUMOylation of p300 (6). Previous studies have demonstrated that SENP1 was able to transform normal prostate epithelium into a dysplasia, and also directly modulate several oncogenic pathways in prostate cells (7,8).…”

Section: Discussionmentioning

confidence: 99%

Detection of differentially expressed genes and association with clinicopathological features in laryngeal squamous cell carcinoma

Shen

Qian

et al. 2012

Oncology Letters

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Abstract. Head and neck cancer is a significant health problem worldwide. Early detection and prediction of prognosis will improve patient survival and quality of life. The aim of this study was to identify genes differentially expressed between laryngeal cancer and the corresponding normal tissues as potential biomarkers. A total of 36 patients with laryngeal squamous cell carcinoma were recruited. Four of these cases were randomly selected for cDNA microarray analysis of the entire genome. Using semi-quantitative RT-PCR and western blot analysis, the differential expression of genes and their protein products, respectively, between laryngeal cancer tissues and corresponding adjacent normal tissues was verified in the remaining 32 cases. The expression levels of these genes and proteins were investigated for associations with clinicopathological parameters taken from patient data. The cDNA microarray analysis identified 349 differentially expressed genes between tumor and normal tissues, 112 of which were upregulated and 237 were downregulated in tumors. Seven genes and their protein products were then selected for validation using RT-PCR and western blot analysis, respectively. The data demonstrated that the expression of SENP1, CD109, CKS2, LAMA3, ITGAV and ITGB8 was increased, while LAMA2 was downregulated in laryngeal cancer compared with the corresponding normal tissues. Associations between the expression of these genes and clinicopathological data from the patients were also established, including age, tumor classification, stage, differentiation and lymph node metastasis. Our current study provides the first evidence that these seven genes may be differentially expressed in laryngeal squamous cell carcinoma and also associated with clinicopathological data.Future study is required to further confirm whether detection of their expression can be used as biomarkers for prediction of patient survival or potential treatment targets. IntroductionHead and neck cancer is the sixth most common type of cancer in the world, accounting for more than 540,000 new cases and 271,000 mortalities each year (1). These cancers occur in the lips, oral cavity, nasal cavity, paranasal sinuses, pharynx and larynx, 90% of which are squamous cell carcinomas. They significantly affect long-term survival and the quality of life of patients. The development of novel strategies is required for prevention and early detection, to reduce cancer incidence and overcome problems associated with treatment of late-stage tumors. Improved prediction of outcome will lead to treatment decisions that prolong patients' survival and quality of life.Predictions concerning the outcome of head and neck cancers are currently based mostly on clinicopathological features, including tumor stage, differentiation, size and regional lymph node or distant metastasis. However, increasing numbers of studies utilize aberrant gene expression and genomic and epigenetic alterations to predict prognosis.It has been established that tobacco smoke and alcohol consump...

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“…prostate Overexpression of SENP1 [131,132] Overexpression of SENP3 [101] colon Overexpression of SENP1 [133] Overexpression of SENP3 [134] liver Downregulation of SENP2 [135] Overexpression of SENP6 [136] bladder Downregulation of SENP2 [137] gastric Overexpression of SENP3 [138] Trends Biochem Sci. Author manuscript; available in PMC 2016 June 01.…”

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

238

211

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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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SUMO-specific protease 1 regulates the in vitro and in vivo growth of colon cancer cells with the upregulated expression of CDK inhibitors

Cited by 76 publications

References 28 publications

SUMOylation regulates p27^Kip1stability and localization in response to TGFβ

SUMOylation regulates p27^Kip1stability and localization in response to TGFβ

Detection of differentially expressed genes and association with clinicopathological features in laryngeal squamous cell carcinoma

SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer

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SUMO-specific protease 1 regulates the in vitro and in vivo growth of colon cancer cells with the upregulated expression of CDK inhibitors

Cited by 76 publications

References 28 publications

SUMOylation regulates p27Kip1stability and localization in response to TGFβ

SUMOylation regulates p27Kip1stability and localization in response to TGFβ

Detection of differentially expressed genes and association with clinicopathological features in laryngeal squamous cell carcinoma

SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer

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SUMOylation regulates p27^Kip1stability and localization in response to TGFβ

SUMOylation regulates p27^Kip1stability and localization in response to TGFβ