<i>UBE2C</i> Is Upregulated by Estrogen and Promotes Epithelial–Mesenchymal Transition via p53 in Endometrial Cancer

Liu, Yan; Zhao, Rong; Chi, Shuqi; Zhang, Wei; Xiao, Chengyu; Zhou, Xing; Zhao, Yingchao; Wang, Hongbo

doi:10.1158/1541-7786.mcr-19-0561

Cited by 81 publications

(74 citation statements)

References 47 publications

(51 reference statements)

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“…Moreover, UBE2C induces Wnt/β-catenin and PI3K/Akt signaling to regulate phosphorylation levels of Aurora-A for epithelial-mesenchymal transition (EMT) in gastric adenocarcinoma [38]. UBE2C promotes EMT via p53 and p21 in endometrial cancer [39]. Our results indicated that UBE2C was involved in cell invasion and migration in OSCC cells ( Figure 3); higher UBE2C expression was associated with lymph node metastasis in OSCC patients ( Supplementary Table S1) and with poor DSS in TSCC patients having lymph node metastasis (Table 3).…”

Section: Discussionmentioning

confidence: 99%

UBE2C is a Potential Biomarker for Tumorigenesis and Prognosis in Tongue Squamous Cell Carcinoma

et al. 2020

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Ubiquitin-conjugating enzyme 2C (UBE2C) involves in numerous cellular processes and the tumor progression in many cancers. However, its role in oral squamous cell carcinoma (OSCC) is unclear. We aimed to investigate the role and clinical significance of UBE2C in OSCC. The expression levels of UBE2C were examined by immunohistochemistry in 185 buccal mucosa squamous cell carcinomas, 247 tongue squamous cell carcinomas (TSCCs) and 75 lip squamous cell carcinomas. The roles of UBE2C in cell growth, invasion/migration and cancer stemness were also examined in OSCC cells. The expression levels of UBE2C protein were higher in tumor tissues than they were in the corresponding tumor adjacent normal tissues from OSCC patients. Higher UBE2C expression was associated with poor cell differentiation and lymph node invasion in OSCC patients. High UBE2C expression was also correlated with shorter disease-specific survival in TSCC patients having poor cell differentiation, advanced pathological stages, lymph node metastasis as well as receiving radiation therapy. Compared to control cells, OSCC cells in which UBE2C was silenced showed decreased cell proliferation, migration/invasion and colony formation and they exhibited lower expression levels of the following cancer stemness markers—ALDH1/A2, CD44, CD166 and EpCAM. High co-expression levels of UBE2C/CD44, UBE2C/CD166 and UBE2C/EpCAM were associated with poor prognosis in oral cancer patients from The Cancer Genome Atlas database. Our findings indicated that UBE2C might be a potential biomarker for tumorigenesis and prognosis in TSCC.

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Section: Discussionmentioning

confidence: 99%

UBE2C is a Potential Biomarker for Tumorigenesis and Prognosis in Tongue Squamous Cell Carcinoma

et al. 2020

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“…Except for physiological structure variation on male and female, the gender-based immunity diversity is showed to account for the difference of sexual hormone secretion, such as estrogen, progestogen and androgen. However, the function of estrogen in cancer research still emphasized on the cancer cell proliferation [ 2 ], angiogenesis [ 3 ], epithelial–mesenchymal transition (EMT) [ 4 ], while the estrogen-induced cancer immune response alternation remains unclear. This review emphasized on the cell modification induced by estrogen and its receptor, estrogen receptor (ER), in canonical and non-canonical manner.…”

Section: Introductionmentioning

confidence: 99%

Estrogen/ER in anti-tumor immunity regulation to tumor cell and tumor microenvironment

Wang¹,

Jin

Qian

et al. 2021

Cancer Cell Int

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As the essential sexual hormone, estrogen and its receptor has been proved to participate in the regulation of autoimmunity diseases and anti-tumor immunity. The adjustment of tumor immunity is related to the interaction between cancer cells, immune cells and tumor microenvironment, all of which is considered as the potential target in estrogen-induced immune system regulation. However, the specific mechanism of estrogen-induced immunity is poorly understood. Typically, estrogen causes the nuclear localization of estrogen/estrogen receptor complex and alternates the transcription pattern of target genes, leading to the reprogramming of tumor cells and differentiation of immune cells. However, the estrogen-induced non-canonical signal pathway activation is also crucial to the rapid function of estrogen, such as NF-κB, MAPK-ERK, and β-catenin pathway activation, which has not been totally illuminated. So, the investigation of estrogen modulatory mechanisms in these two manners is vital for the tumor immunity and can provide the potential for endocrine hormone targeted cancer immunotherapy. Here, this review summarized the estrogen-induced canonical and non-canonical signal transduction pathway and aimed to focus on the relationship among estrogen and cancer immunity as well as immune-related tumor microenvironment regulation. Results from these preclinical researches elucidated that the estrogen-target therapy has the application prospect of cancer immunotherapy, which requires the further translational research of these treatment strategies.

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“…This indicates that Ube2c may have a multi-directional promotion effect on hepatocyte proliferation. Studies on the mechanism of UBE2C expression indicate that the expression of UBE2C may be stimulated by androgen- or estrogen-receptor, lncRNA and miRNA ( Kato et al, 2016 ; Gu et al, 2017 ; Hu et al, 2019 ; Liu et al, 2020 ). These provide a general direction for us to further study the reasons for the up-regulation of Ube2c in the early stage of liver regeneration.…”

Section: Discussionmentioning

confidence: 99%

Identifying the Key Genes in Mouse Liver Regeneration After Partial Hepatectomy by Bioinformatics Analysis and in vitro/vivo Experiments

Zhao

Cai

et al. 2021

Front. Genet.

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BackgroundThe liver is the only organ that can completely regenerate after various injuries or tissue loss. There are still a large number of gene functions in liver regeneration that have not been explored. This study aimed to identify key genes in the early stage of liver regeneration in mice after partial hepatectomy (PH).Materials and MethodsWe first analyzed the expression profiles of genes in mouse liver at 48 and 72 h after PH from Gene Expression Omnibus (GEO) database. Gene ontology (GO), and the Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein–protein interaction (PPI) analysis were performed to identify key genes in liver regeneration. Finally, we validated key genes in vivo and in vitro.ResultsWe identified 46 upregulated genes and 19 downregulated genes at 48 h after PH, and 223 upregulated genes and 40 downregulated genes at 72 h after PH, respectively. These genes were mainly involved in cell cycle, DNA replication, and p53 signaling pathway. Among of these genes, cycle-related genes (Ccna2, Cdkn1a, Chek1, and Mcm5) and Ube2c were highly expressed in the residual liver both at 48 and 72 h after PH. Furthermore, Ube2c knockdown not only caused abnormal expression of Ccna2, Cdkn1a, Chek1, and Mcm5, but also inhibited transition of hepatocytes from G1 to S phase of the cell cycle in vitro.ConclusionMouse hepatocytes enter the proliferation phase at 48 h after PH. Ube2c may mediate cell proliferation by regulating or partially regulating Ccna2, Cdkn1a, Chek1, and Mcm5.

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UBE2C Is Upregulated by Estrogen and Promotes Epithelial–Mesenchymal Transition via p53 in Endometrial Cancer

Cited by 81 publications

References 47 publications

UBE2C is a Potential Biomarker for Tumorigenesis and Prognosis in Tongue Squamous Cell Carcinoma

UBE2C is a Potential Biomarker for Tumorigenesis and Prognosis in Tongue Squamous Cell Carcinoma

Estrogen/ER in anti-tumor immunity regulation to tumor cell and tumor microenvironment

Identifying the Key Genes in Mouse Liver Regeneration After Partial Hepatectomy by Bioinformatics Analysis and in vitro/vivo Experiments

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