UBE2T promotes glioblastoma invasion and migration via stabilizing GRP78 and regulating EMT

Huang, Peng; Guo, Yunbo; Zhao, Zitong; Ning, Weihai; Wang, Haoran; Li, Zhuoshi; Zhang, Mingshan; Qu, Yanming; Zhang, Hongwei; Song, Yongmei

doi:10.18632/aging.103239

Cited by 28 publications

(27 citation statements)

References 38 publications

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“…Besides HMMR, the other four hub genes (UBE2T, PTTG1, GINS2 and TYMS) have been shown to play a role in HCC. UBE2T, a member of the E2 family, is demonstrated to be a vital regulator of tumor progression in several cancers, such as lung cancer [63], glioblastoma [64], and HCC [65]. PTTG1 has been reported to be associated with poor prognosis in multiple myeloma [66], prostate cancer [67] and HCC [68].…”

Section: Discussionmentioning

confidence: 99%

Oleate acid-stimulated HMMR expression by CEBPα is associated with nonalcoholic steatohepatitis and hepatocellular carcinoma

Zhang¹,

Liu²,

Xie³

et al. 2020

Int. J. Biol. Sci.

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Non-alcoholic steatohepatitis (NASH) is a type of nonalcoholic fatty liver disease and has become a major risk factor for hepatocellular carcinoma (HCC). However, the underlying pathophysiological mechanisms are still elusive. Here, we identify hyaluronan-mediated motility receptor (HMMR) as a critical gene associated with NASH/HCC by combination of bioinformatic analysis and functional experiments. Analysis of differentially expressed genes (DEGs) between normal controls and NASH/HCC identified 5 hub genes (HMMR, UBE2T, TYMS, PTTG1 and GINS2). Based on the common DEGs, analyses of univariate and multivariate Cox regression and the area under the curve (AUC) value of the receiver operating characteristic (ROC) indicate that HMMR is the most significant gene associated with NASH/HCC among five hub genes. Oleate acid (OA), one of fatty acids that induce cellular adipogenesis, stimulates HMMR expression via CCAAT/enhancer-binding protein α (CEBPα). CEBPα increases the expression of HMMR through binding to its promoter. HMMR promotes HCC cell proliferation in vitro via activation of G1/S and G2/M checkpoint transitions, concomitant with a marked increase of the positive cell cycle regulators, including cyclin D1, cyclin E, and cyclin B1. Knockdown of HMMR suppresses HCC tumor growth in nude mice. Our study identifies an important role of HMMR in NASH/HCC, and suggests that HMMR may be a useful target for therapy and prognostic prediction of NASH/HCC patients.

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Section: Discussionmentioning

confidence: 99%

Oleate acid-stimulated HMMR expression by CEBPα is associated with nonalcoholic steatohepatitis and hepatocellular carcinoma

Zhang¹,

Liu²,

Xie³

et al. 2020

Int. J. Biol. Sci.

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“…Silencing UBE2C causes pancreatic ductal adenocarcinoma cells to block in the G1/S phase, and reduces the levels of EMT markers (VIM, E-cadherin) [ 182 ]. E2s that regulate EMT also include UBE2O, UBE2V1, and UBE2T [ 183 ]. Flavopiridol can significantly inhibit the activity of CDKs (1/2/4/6/7) by interacting with the ATP binding pocket on the kinase, thereby causing G1/G2/M phase block.…”

Section: Biological Processes Involving E2smentioning

confidence: 99%

The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy

Song

Shen

et al. 2021

IJMS

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Ubiquitin-conjugating enzymes (E2s) are one of the three enzymes required by the ubiquitin-proteasome pathway to connect activated ubiquitin to target proteins via ubiquitin ligases. E2s determine the connection type of the ubiquitin chains, and different types of ubiquitin chains regulate the stability and activity of substrate proteins. Thus, E2s participate in the regulation of a variety of biological processes. In recent years, the importance of E2s in human health and diseases has been particularly emphasized. Studies have shown that E2s are dysregulated in variety of cancers, thus it might be a potential therapeutic target. However, the molecular basis of E2s as a therapeutic target has not been described systematically. We reviewed this issue from the perspective of the special position and role of E2s in the ubiquitin-proteasome pathway, the structure of E2s and biological processes they are involved in. In addition, the inhibitors and microRNAs targeting E2s are also summarized. This article not only provides a direction for the development of effective drugs but also lays a foundation for further study on this enzyme in the future.

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“…In addition, knockdown of UBE2T could inhibit cell proliferation and invasion via regulating the PI3K/Akt signaling pathway in osteosarcoma (10). UBE2T have reported to accelerate glioblastoma invasion via regulating GRP78 (11). Yin et al found that UBE2T promotes epithelial-mesenchymal transition through mediating FOXO1 degradation in non-small cell lung cancer (12).…”

Section: Introductionmentioning

confidence: 99%

UBE2T knockdown inhibits cell growth and metastasis of breast cancer through Wnt/β-catenin pathway

Xueqin¹,

Mei²,

Yuping³

2021

Preprint

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Background: Emerging evidences have demonstrated that Ubiquitin-conjugating enzyme E2T (UBE2T) is dysregulated and play critical roles in various cancers. With the development of sequencing technology, studies have discovered that UBE2T is overexpressed in breast cancer tissues. However, the biological roles of UBE2T in breast cancer are still far to clear. In the present study, Methods: We analyzed the UBE2T expression in the Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to assess the expression of UBE2T in breast cancer cell lines. Cell proliferation, invasion and epithelial-mesenchymal transition (EMT) were determined by using CCK-8, EdU, Transwell and western blot assays.Results: UBE2T was highly expressed in breast cancer cell lines. Functional analysis revealed that silence or elevation of UBE2T inhibited or promoted the proliferation, migration, invasion and EMT and Wnt/β-catenin signaling pathway related markers of MCF-7 cells. Mechanically, blocking of Wnt/β-catenin pathway by XAV939 reversed the promotion effect of UBE2T overexpression on breast cancer cells’ proliferation, migration and invasion.Conclusion: Our findings emphasized that UBE2T may act as an oncogene via activating the Wnt/β-catenin pathway, which may provide a potential therapeutic target for the treatment of breast cancer.

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UBE2T promotes glioblastoma invasion and migration via stabilizing GRP78 and regulating EMT

Cited by 28 publications

References 38 publications

Oleate acid-stimulated HMMR expression by CEBPα is associated with nonalcoholic steatohepatitis and hepatocellular carcinoma

Oleate acid-stimulated HMMR expression by CEBPα is associated with nonalcoholic steatohepatitis and hepatocellular carcinoma

The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy

UBE2T knockdown inhibits cell growth and metastasis of breast cancer through Wnt/β-catenin pathway

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