YY1 expression and PD-1 regulation in CD8 T lymphocytes

Touboul, Roni; Bonavida, Benjamin

doi:10.1016/b978-0-12-821909-6.00003-1

Cited by 3 publications

(12 citation statements)

References 156 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Death receptors in cancer cells are induced by RKIP because of RKIP’s ability to inhibit the NF-kB/YY1 cascade. YY1 is a multifunctional zinc-finger transcription factor that regulates several cellular functions including, but not limited to, B-cell development, proliferation, tumorigenesis, and differentiation [ 206 , 207 , 208 , 209 ]. As a member of the polycomb group (PcG) of proteins, it can work together with other members of the complex [ 206 , 207 , 210 , 211 , 212 , 213 ].…”

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

“…YY1 is a multifunctional zinc-finger transcription factor that regulates several cellular functions including, but not limited to, B-cell development, proliferation, tumorigenesis, and differentiation [ 206 , 207 , 208 , 209 ]. As a member of the polycomb group (PcG) of proteins, it can work together with other members of the complex [ 206 , 207 , 210 , 211 , 212 , 213 ]. YY1 represses the transcription of some of these death receptors, including death receptor 5 (DR5) and Fas in different tumor types [ 12 , 214 , 215 ].…”

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

“…Lag3, TIM) and their interactions with corresponding ligands on the tumor cells [ 228 ]. Using a gel shift assay and reporter gene assays, it was confirmed that YY1 binds to the promoters of PD-1 and Lag3 and that there is increased transcription with repeat T-cell stimulation that is caused by a mutation in the YY1 binding sites [ 206 , 207 , 229 ]. This confirmed that PD-1 and Lag3 are positively regulated by YY1.…”

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

“…This confirmed that PD-1 and Lag3 are positively regulated by YY1. This was further studied using a luciferase reporter assay that showed an increase in PD-1 in CD8 T cells that contained functional YY1 binding sites as opposed to the decrease or loss of activity when YY1 binding sites were mutated [ 206 , 207 ]. Therefore, RKIP’s inhibition of YY1 leads to a decrease in the expression of PD-1.…”

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

“…In addition, YY1 was identified as a transcription factor for PD-1 and it was found to be highly expressed in melanoma exhausted PD-1 + T cells [ 206 , 207 , 230 ]. This further suggests that the inhibition of YY1 in tumor cells should lead to the inhibition of PD-1 expression in lymphocytes [ 206 , 230 ].…”

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

See 4 more Smart Citations

RKIP Pleiotropic Activities in Cancer and Inflammatory Diseases: Role in Immunity

Touboul

Baritaki

Zaravinos

et al. 2021

Cancers

Self Cite

View full text Add to dashboard Cite

Several gene products play pivotal roles in the induction of inflammation and the progression of cancer. The Raf kinase inhibitory protein (RKIP) is a cytosolic protein that exerts pleiotropic activities in such conditions, and thus regulates oncogenesis and immune-mediated diseases through its deregulation. Herein, we review the general properties of RKIP, including its: (i) molecular structure; (ii) involvement in various cell signaling pathways (i.e., inhibition of the Raf/MEK/ERK pathway; the NF-kB pathway; GRK-2 or the STAT-3 pathway; as well as regulation of the GSK3Beta signaling; and the spindle checkpoints); (iii) regulation of RKIP expression; (iv) expression’s effects on oncogenesis; (v) role in the regulation of the immune system to diseases (i.e., RKIP regulation of T cell functions; the secretion of cytokines and immune mediators, apoptosis, immune check point inhibitors and RKIP involvement in inflammatory diseases); and (vi) bioinformatic analysis between normal and malignant tissues, as well as across various immune-related cells. Overall, the regulation of RKIP in different cancers and inflammatory diseases suggest that it can be used as a potential therapeutic target in the treatment of these diseases.

show abstract

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

Section: Rkip–immune System Cross-talksmentioning

confidence: 99%

See 3 more Smart Citations

RKIP Pleiotropic Activities in Cancer and Inflammatory Diseases: Role in Immunity

Touboul

Baritaki

Zaravinos

et al. 2021

Cancers

Self Cite

View full text Add to dashboard Cite

show abstract

Emerging Role of PD-1/PD-L1 Inhibitors in Chronic Liver Diseases

et al. 2021

View full text Add to dashboard Cite

Programmed cell death protein 1 (PD-1)/PD-ligand (L)1, the immune checkpoint inhibitors have emerged as a promising strategy for the treatment of various diseases including chronic liver diseases (CLDs) such as hepatitis, liver injury and hepatocellular carcinoma (HCC). The role of PD-1/PD-L1 has been widely inspected in the treatment of viral hepatitis and HCC. PD-1 is known to play a crucial role in inhibiting immunological responses and stimulates self-tolerance by regulating the T-cell activity. Further, it promotes apoptosis of antigen-specific T-cells while preventing apoptosis of Treg cells. PD-L1 is a trans-membrane protein which is recognized as a co-inhibitory factor of immunological responses. Both, PD-1 and PD-L1 function together to downregulate the proliferation of PD-1 positive cells, suppress the expression of cytokines and stimulate apoptosis. Owing to the importance of PD-1/PD-L1 signaling, this review aims to summarize the potential of PD-1/PD-L1 inhibitors in CLDs along with toxicities associated with them. We have enlisted some of the important roles of PD-1/PD-L1 in CLDs, the clinically approved products and the pipelines of drugs under clinical evaluation.

show abstract

An Updated Review of the Biomarkers of Response to Immune Checkpoint Inhibitors in Merkel Cell Carcinoma: Merkel Cell Carcinoma and Immunotherapy

Fojnica,

Ljuca,

Akhtar

et al. 2023

Cancers

View full text Add to dashboard Cite

Merkel cell carcinoma (MCC) is primarily a disease of the elderly Caucasian, with most cases occurring in individuals over 50. Immune checkpoint inhibitors (ICI) treatment has shown promising results in MCC patients. Although ~34% of MCC patients are expected to exhibit at least one of the predictive biomarkers (PD-L1, high tumor mutational burden/TMB-H/, and microsatellite instability), their clinical significance in MCC is not fully understood. PD-L1 expression has been variably described in MCC, but its predictive value has not been established yet. Our literature survey indicates conflicting results regarding the predictive value of TMB in ICI therapy for MCC. Avelumab therapy has shown promising results in Merkel cell polyomavirus (MCPyV)-negative MCC patients with TMB-H, while pembrolizumab therapy has shown better response in patients with low TMB. A study evaluating neoadjuvant nivolumab therapy found no significant difference in treatment response between the tumor etiologies and TMB levels. In addition to ICI therapy, other treatments that induce apoptosis, such as milademetan, have demonstrated positive responses in MCPyV-positive MCC, with few somatic mutations and wild-type TP53. This review summarizes current knowledge and discusses emerging and potentially predictive biomarkers for MCC therapy with ICI.

show abstract

YY1 expression and PD-1 regulation in CD8 T lymphocytes

Cited by 3 publications

References 156 publications

RKIP Pleiotropic Activities in Cancer and Inflammatory Diseases: Role in Immunity

RKIP Pleiotropic Activities in Cancer and Inflammatory Diseases: Role in Immunity

Emerging Role of PD-1/PD-L1 Inhibitors in Chronic Liver Diseases

An Updated Review of the Biomarkers of Response to Immune Checkpoint Inhibitors in Merkel Cell Carcinoma: Merkel Cell Carcinoma and Immunotherapy

Contact Info

Product

Resources

About