Induction and Regulation of the Immunoproteasome Subunit β5i (PSMB8) in Laryngeal and Hypopharyngeal Carcinoma Cells

Nan-xiang, Chen; Liu, Kun; Li, Xuan; Zhang, Xinxin; Han, Dongyi

doi:10.12659/msm.923621

Cited by 5 publications

(6 citation statements)

References 27 publications

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“…Indeed, PSMB8 has demonstrated its involvement in autoimmune disease, lipodystrophy, lipid metabolic disorders, and diabetes mellitus 15 . In addition, PSMB8 was reported to be responsible for cell growth and proliferation activities 39 . Therefore, the common IP inhibitor ONX-0914, used for treating some conditions such as in ammatory diseases, is the selective LMP7 (PSMB8) inhibitor 15,40 .…”

Section: Discussionmentioning

confidence: 99%

Alteration of immunoproteasome mRNA in PBMCs of patients with Parkinson’s disease

Kim

Nguyen

et al. 2022

Preprint

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Background Immunoproteasome, a part of ubiquitin–proteasome system, is involved in protein degradation and immune response. However, the relationship between immunoproteasome and Parkinson’s disease (PD) was not evaluated clearly. We hypothesized that the shift of immunoproteasome attributes to PD due to its role in immune system and protein homeostasis. Objective To determine whether immunoproteasome mRNA in peripheral blood mononuclear cells is expressed differently between patients with PD and healthy controls and to test its value as a biomarker of PD Methods Blood samples were collected from 19 healthy controls and 40 patients with PD of comparable ages. Peripheral blood mononuclear cells were isolated and used to measure by RT-qPCR the mRNA levels of three catalytic subunits of immunoproteasome, namely, PSMB8, PSMB9, and PSMB10. Results The levels PSMB9 and PSMB10 mRNA were not different between the PD group and healthy control group, whereas the PSMB8 mRNA in PD group significantly increased. The ratio of PSMB10 and PSMB8 (PSMB10/8) best reflected significant difference between the PD group and healthy control group (p = 0.002). This ratio can discriminate all PD, mild PD (Hoehn and Yahr ≤ 2.5), and drug-naive PD from healthy controls. We found correlation between the PSMB10/8 ratio with the UPDRS total and Part III score in the mild PD subgroup and drug-naive PD subgroups Conclusion The expression of PSMB8 mRNA increased in PD, and the PSMB10/8 ratio can differentiate Parkinson’s disease from healthy controls.

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Section: Discussionmentioning

confidence: 99%

Alteration of immunoproteasome mRNA in PBMCs of patients with Parkinson’s disease

Kim

Nguyen

et al. 2022

Preprint

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“…Immunoproteasome has been the subject of several studies due to its role in the differentiation of T cells, cytokine regulation, and tumor progression (Chen et al, 2020;Kiuchi et al, 2021;Zerfas et al, 2020). In addition, it is known that the peptides generated by the immunoproteasome for MHC class I are capable of generating a more efficient and accentuated cytotoxic lymphocyte response than those generated by the constitutive proteasome, contributing to CD8+ T cell infiltration (Groettrup et al, 2001;Kloetzel, 2001).…”

Section: Discussionmentioning

confidence: 99%

Oral Lichen Planus and its relation with Oral Squamous Cell Carcinoma: new insights into the potential for malignant transformation

et al. 2021

Preprint

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Oral Lichen Planus (OLP) is a chronic inflammatory disorder of unknown etiology. However, evidence suggests that it consists of an immunological process that leads to degeneration of the keratinocytes in the basal layer of the oral mucosa. Despite being recognized by WHO as a potentially malignant disorder with progression to oral squamous cell carcinoma (OSCC), the relationship between both pathologies is still controversial. Different studies have investigated factors associated with the potential for malignant transformation of OLP but it remains unclear. Through a bioinformatics approach, we investigated similarities in gene expression profiles of OLP and OSCC in early and advanced stages. Our results revealed gene expression patterns related to processes of keratinization, keratinocyte differentiation, cell proliferation and immune response in common between OLP and early and advanced OSCC, with the cornified envelope formation and antigen processing cross-presentation pathways in common between OLP and early OSCC. Together, these results reveal that key genes such as PI3, SPRR1B and KRT17, in addition to genes associated with different immune processes such as CXCL-13, HIF1A and IL1B may be involved in this oncogenic process. In addition, we performed an analysis of differentially and co-expressed genes and proposed putative therapeutic targets and associated drugs.

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“…Treatment of AD model Tg2576 mice with nilotinib reduces c-Abl phosphorylation/activation and enhances autophagy, leading to a reduction in Aβ levels and preventing degeneration of dopaminergic neurons [ 2 ]. With regard to the ubiquitin-proteasome pathway in proliferating cells, silencing of the Abl gene and activation/inhibition of c-Abl kinase activity have been shown to affect expression levels of the proteasome subunit beta-type 8 precursor (PSMB8) and its alternatively spliced isoforms [ 114 ].…”

Section: C-abl and Autophagymentioning

confidence: 99%

The Role of c-Abl Tyrosine Kinase in Brain and Its Pathologies

Motaln

Rogelj

2023

Cells

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Differentiated status, low regenerative capacity and complex signaling make neuronal tissues highly susceptible to translating an imbalance in cell homeostasis into cell death. The high rate of neurodegenerative diseases in the elderly population confirms this. The multiple and divergent signaling cascades downstream of the various stress triggers challenge researchers to identify the central components of the stress-induced signaling pathways that cause neurodegeneration. Because of their critical role in cell homeostasis, kinases have emerged as one of the key regulators. Among kinases, non-receptor tyrosine kinase (Abelson kinase) c-Abl appears to be involved in both the normal development of neural tissue and the development of neurodegenerative pathologies when abnormally expressed or activated. However, exactly how c-Abl mediates the progression of neurodegeneration remains largely unexplored. Here, we summarize recent findings on the involvement of c-Abl in normal and abnormal processes in nervous tissue, focusing on neurons, astrocytes and microglial cells, with particular reference to molecular events at the interface between stress signaling, DNA damage, and metabolic regulation. Because inhibition of c-Abl has neuroprotective effects and can prevent neuronal death, we believe that an integrated view of c-Abl signaling in neurodegeneration could lead to significantly improved treatment of the disease.

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Induction and Regulation of the Immunoproteasome Subunit β5i (PSMB8) in Laryngeal and Hypopharyngeal Carcinoma Cells

Cited by 5 publications

References 27 publications

Alteration of immunoproteasome mRNA in PBMCs of patients with Parkinson’s disease

Alteration of immunoproteasome mRNA in PBMCs of patients with Parkinson’s disease

Oral Lichen Planus and its relation with Oral Squamous Cell Carcinoma: new insights into the potential for malignant transformation

The Role of c-Abl Tyrosine Kinase in Brain and Its Pathologies

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