Ubiquitin-conjugating enzyme E2 B regulates the ubiquitination of O-methylguanine-DNA methyltransferase and BCNU sensitivity in human nasopharyngeal carcinoma cells

Hsu, Shu-Hau; Chen, Shang Hung; Kuo, Ching Chuan; Chang, Jang Yang

doi:10.1016/j.bcp.2018.10.029

Cited by 13 publications

(27 citation statements)

References 48 publications

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“…The overview of the CIK cell preparation schedule was shown in Figure 1A. Consistent with a previous study [21], we also found that activated CIK cells aggregated together to form clusters. These CIK cell clusters were first observed on the third day after induction, increased rapidly during the first seven days and continued to the fourteenth day of induction (Figure 1B).…”

Section: Activation and Expansion Of Cik Cellssupporting

confidence: 90%

“…Human peripheral blood mononuclear cells (PBMCs) were isolated by Ficoll-Hypaque (GE Healthcare) density-gradient centrifugation and then washed three times and plated into 25 cm 2 flasks at a concentration of 2 × 10 6 cells/ml in X-VIVO 15 hematopoietic medium (Lonza, 04-418Q) containing human IFN-γ (#300-02, PeproTech). On the next day, anti-CD3 monoclonal antibody (clone OKT3; 16-0037-85, eBioscience) and IL-2 (#200-02, PeproTech) were added to the medium [21]. Cells were incubated in a humidified atmosphere with 5% CO 2 at 37 • C and changed medium every 2-3 days.…”

Section: Cik Cell Preparationmentioning

confidence: 99%

“…In recent years, many studies indicate that cancer immunotherapy may be another choice for cancer treatment [12][13][14][15][16][17][18][19][20][21][22]. Different to surgery, chemotherapy and radiotherapy, immunotherapy focuses on improving the anti-cancer abilities of immune cells and promoting the patient's own immune system to fight diseases [18,20,23,24].…”

Section: Introductionmentioning

confidence: 99%

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Impact of FAK Expression on the Cytotoxic Effects of CIK Therapy in Triple-Negative Breast Cancer

Pan

Kan

et al. 2019

Cancers

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Triple-negative breast cancer (TNBC) is a special subtype of breast cancer in which several common diagnostic biomarkers are lost. Due to the loss of expression of receptors, treatment options for TNBC are limited. Therefore, finding safe and effective treatments for patients with TNBC is a major objective for clinicians. Previous studies suggested that cytokine-induced killer (CIK) cells may be beneficial for patients with a variety of tumor types. However, CIK therapy is not effective for all patients. In this study, we found that focal adhesion kinase (FAK), a non-receptor protein tyrosine kinase that regulates several cellular functions in different cells, has the potential to regulate tumor cells sensitized to CIK cells. Knockdown of FAK expression in TNBC cells or the treatment of TNBC cells with a FAK inhibitor followed by coculture with CIK cells increases death of TNBC cells, suggesting that FAK plays important roles in sensitizing tumor cells to CIK cells. This phenomenon could be regulated by a FAK-programmed death-ligand 1 (PD-L1)-related mechanism. Overall, our findings provide new insights into the cytotoxic effect of CIK cell therapy in TNBC treatment, and show that CIK cell therapy combined with FAK inhibitors may be a novel therapeutic strategy for patients with TNBC.

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Section: Activation and Expansion Of Cik Cellssupporting

confidence: 90%

Section: Cik Cell Preparationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impact of FAK Expression on the Cytotoxic Effects of CIK Therapy in Triple-Negative Breast Cancer

Pan

Kan

et al. 2019

Cancers

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“…179 183 Research findings showed that ubiquitinconjugating enzyme E2 B (UBE2B) collaborates with E3 ubiquitin ligase RAD18 to mediated MGMT ubiquitination and degradation. 184 Rad18 is also responsible for monoubiquitination of PCNA, which initiates several cellular DNA repair processes. V-DUB BPLF1 targets ubiquitinated PCNA and disrupts trans-lesion synthesis (TLS).…”

Section: Ebv and The Ubiquitin-proteasome System (Ups)mentioning

confidence: 99%

Targeting the signaling in Epstein–Barr virus-associated diseases: mechanism, regulation, and clinical study

Cao

Xie

Shi

et al. 2021

Sig Transduct Target Ther

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Epstein–Barr virus-associated diseases are important global health concerns. As a group I carcinogen, EBV accounts for 1.5% of human malignances, including both epithelial- and lymphatic-originated tumors. Moreover, EBV plays an etiological and pathogenic role in a number of non-neoplastic diseases, and is even involved in multiple autoimmune diseases (SADs). In this review, we summarize and discuss some recent exciting discoveries in EBV research area, which including DNA methylation alterations, metabolic reprogramming, the changes of mitochondria and ubiquitin-proteasome system (UPS), oxidative stress and EBV lytic reactivation, variations in non-coding RNA (ncRNA), radiochemotherapy and immunotherapy. Understanding and learning from this advancement will further confirm the far-reaching and future value of therapeutic strategies in EBV-associated diseases.

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“…Their importance in tumorigenesis has been revealed by a series of studies. UBE2S was found to be involved in lung adenocarcinoma and hepatocellular carcinoma by regulating the p53 signaling pathway (22,23), while UBE2D1, UBE2B, UBE2V1, and UBE2Q1 were shown to be involved in hepatocellular carcinoma, nasopharyngeal carcinoma, and colorectal cancer (24)(25)(26)(27) by regulating oncogenes or tumor suppressors. This demonstrates the key roles of the UBE2 family in tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

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

Liu

Zhao

Chi

et al. 2020

Molecular Cancer Research

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Ubiquitin-conjugating enzyme E2C (UBE2C) plays important roles in tumor progression; nevertheless, its function in endometrial cancer remains unclear. This study elucidated the impact of UBE2C on endometrial cancer and its underlying mechanism. Human endometrial cancer and normal endometrial tissues were acquired from patients at Wuhan Union Hospital and UBE2C expression was detected by Western blotting and qRT-PCR. Endometrial cancer cells were transfected with a UBE2C overexpression plasmid or UBE2C-specific short hairpin RNA (shRNA) to up-or downregulate UBE2C expression, respectively. CCK8 and transwell assays were applied to assess the effects of UBE2C on cell proliferation, migration, and invasion. We found a significant elevation of UBE2C expression in patients with endometrial cancer, and that UBE2C upregulation was associated with advanced histologic grade, FIGO stage, recurrence, and shorter overall survival. UBE2C knockdown inhibited endometrial cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), whereas UBE2C overexpression exerted the opposite effects. UBE2C downregulation increased p53 and its downstream p21 expression, with p53 overexpression reversing the EMT-promoting effects of UBE2C. UBE2C enhanced p53 ubiquitination to facilitate its degradation in endometrial cancer cells. Estradiol (E2) induced UBE2C expression via estrogen receptor a, which binds directly to the UBE2C promoter element. Silencing of UBE2C inhibited E2-promoted migration, invasion, and EMT in vitro and in vivo.Implications: UBE2C-mediated tumor EMT promotion by estrogen is a novel mechanism for the progression of estrogen-induced endometrial cancer, which could offer new biomarkers for diagnosis and therapy of endometrial cancer in the future.

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Ubiquitin-conjugating enzyme E2 B regulates the ubiquitination of O-methylguanine-DNA methyltransferase and BCNU sensitivity in human nasopharyngeal carcinoma cells

Cited by 13 publications

References 48 publications

Impact of FAK Expression on the Cytotoxic Effects of CIK Therapy in Triple-Negative Breast Cancer

Impact of FAK Expression on the Cytotoxic Effects of CIK Therapy in Triple-Negative Breast Cancer

Targeting the signaling in Epstein–Barr virus-associated diseases: mechanism, regulation, and clinical study

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

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