Roles of Ubiquitination and SUMOylation in the Regulation of Angiogenesis

Rabellino, Andrea; Andreani, Cristina; Scaglioni, Pier Paolo

doi:10.21775/cimb.035.109

Cited by 7 publications

(3 citation statements)

References 138 publications

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“…In addition, relevant literature has shown that the ubiquitination of UBE2C can regulate angiogenesis by regulating VEGFR, NOTCH signaling, and WNT signaling, among others. 34 Zhang et al found that AGGF1 promotes angiogenesis by regulating the PI3K–AKT pathway in mice. 20 However, further experiments are required to identify the pathways through which UBE2C and AGGF1 promote angiogenesis in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

The Relationship Between UBE2C and AGGF1 Overexpression and Tumor Angiogenesis in Non-Small Cell Lung Cancer

Wang¹,

Shi²,

Tao³

et al. 2021

CMAR

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Background Tumor infiltration and metastasis are the leading causes of death for patients with tumors. Angiogenesis is a prerequisite for tumor growth and metastasis. Angiogenic factor with G patch and FHA domains 1 (AGGF1) is an angiogenic factor, whereas ubiquitin-conjugating enzyme E2C (UBE2C) functions in protein ubiquitination. Microvessel density (MVD) is the most common indicator of tumor microvessels, and vasculogenic mimicry (VM) facilitates blood supply to tumors. This study explored UBE2C and AGGF1 expression in non-small cell lung cancer (NSCLC) and their relationship with angiogenesis and prognosis to identify biological factors that might predict NSCLC infiltration, metastasis, and prognosis. Methods The specimens and clinical pathological data of patients with NSCLC confirmed by pathology after surgical resection between January 2013 and December 2015 were collected. UBE2C and AGGF1 expression, as well as microvessel formation and VM in NSCLC, was observed using immunohistochemistry. The relationships between UBE2C, AGGF1, MVD, VM, and clinical pathological parameters and their relationships with overall survival (OS) and disease-free survival (DFS) were analyzed. Results UBE2C and AGGF1 levels in NSCLC tissues were significantly higher than those in corresponding normal tissues (57.1% vs 15.6 and 59.7% vs 25.3%, respectively; P < 0.05). UBE2C, AGGF1, MVD, and VM were positively correlated with each other ( P < 0.05) and were all related to tumor size, lymph node metastasis, and tumor-node-metastasis stage ( P < 0.05). Kaplan–Meier analysis showed that patient OS and DFS in the UBE2C, AGGF1, VM-positive, and high-MVD groups were reduced (all P < 0.001). Univariate and multivariate analyses showed that UBE2C, AGGF1, VM, and MVD were independent risk factors for NSCLC prognosis. Conclusion UBE2C and AGGF1 overexpression is associated with angiogenesis and poor prognosis and may be important for predicting NSCLC invasion, metastasis, and prognosis.

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Section: Discussionmentioning

confidence: 99%

The Relationship Between UBE2C and AGGF1 Overexpression and Tumor Angiogenesis in Non-Small Cell Lung Cancer

Wang¹,

Shi²,

Tao³

et al. 2021

CMAR

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show abstract

“…Angiogenesis and Metastasis. E1-initiated posttranslational modifications have been reported to regulate angiogenesis via direct and indirect mechanisms (Rahimi, 2012;Rabellino et al, 2020). In this respect, vascular endothelial growth factor receptor signaling is known to be regulated by ubiquitylation and SUMOylation (Simons et al, 2016;Zhou et al, 2018).…”

Section: E Biologic Functions Of E1 Enzymes and Their Implications In Cancer Therapymentioning

confidence: 99%

E1 Enzymes as Therapeutic Targets in Cancer

Barghout¹,

Schimmer²

2020

Pharmacol Rev

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“…Tip cells secrete the Notch ligand Dll4 which binds to the Notch receptor on stalk cells. The activation of Notch leads to VEGFR2 transcriptional inhibition and subsequently suppresses endothelial cell proliferation ( 44 ). Ubiquitin ligase F-box and WD repeat domain-containing 7 (FBW7) plays a positive role in angiogenesis by inducing Notch ubiquitination and degradation ( 45 ).…”

Section: Roles Of Ubiquitination In Modulating the Crosstalk Between ...mentioning

confidence: 99%

Roles of ubiquitination in the crosstalk between tumors and the tumor microenvironment (Review)

et al. 2022

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The interaction between a tumor and the tumor microenvironment (TME) plays a key role in tumorigenesis and tumor progression. Ubiquitination, a crucial post-translational modification for regulating protein degradation and turnover, plays a role in regulating the crosstalk between a tumor and the TME. Thus, identifying the roles of ubiquitination in the process may assist researchers to investigate the mechanisms underlying tumorigenesis and tumor progression. In the present review article, new insights into the substrates for ubiquitination that are involved in the regulation of hypoxic environments, angiogenesis, chronic inflammation-mediated tumor formation, and the function of cancer-associated fibroblasts and infiltrating immune cells (tumor-associated macrophages, T-cells, myeloid-derived suppressor cells, dendritic cells, and natural killer cells) are summarized. In addition, the potential targets of the ubiquitination proteasome system within the TME for cancer therapy and their therapeutic effects are reviewed and discussed.

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Roles of Ubiquitination and SUMOylation in the Regulation of Angiogenesis

Cited by 7 publications

References 138 publications

The Relationship Between UBE2C and AGGF1 Overexpression and Tumor Angiogenesis in Non-Small Cell Lung Cancer

The Relationship Between UBE2C and AGGF1 Overexpression and Tumor Angiogenesis in Non-Small Cell Lung Cancer

E1 Enzymes as Therapeutic Targets in Cancer

Roles of ubiquitination in the crosstalk between tumors and the tumor microenvironment (Review)

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