Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Existing studies have underscored the pivotal role of N-acetyltransferase 10(NAT10)in various cancers.However,the outcomes of protein-protein interactions between NAT10 and its protein partners in head and neck squamous cell carcinoma(HNSCC)remain unexplored.In this study,we identified a significant upregulation of RNA-binding protein with serine-rich domain 1(RNPS1)in HNSCC,where RNPS1 inhibits the ubiquitination degradation of NAT10 by E3 ubiquitin ligase,zinc finger SWIM domain-containing protein 6(ZSWIM6),through direct protein interaction,thereby promoting high NAT10 expression in HNSCC.This upregulated NAT10 stability mediates the enhancement of specific tRNA ac4C modifications,subsequently boosting the translation process of genes involved in pathways such as IL-6 signaling,IL-8 signaling,and PTEN signaling that play roles in regulating HNSCC malignant progression,ultimately influencing the survival and prognosis of HNSCC patients.Additionally,we pioneered the development of TRMC-seq,leading to the discovery of novel tRNA-ac4C modification sites,thereby providing a potent sequencing tool for tRNA-ac4C research.Our findings expand the repertoire of tRNA ac4C modifications and identify a role of tRNA ac4C in the regulation of mRNA translation in HNSCC.

Head and neck squamous cell carcinoma(HNSCC)is characterized by high recurrence or distant metastases rate and the prognosis is challenging.There is mounting evidence that tumor-infiltrating B cells(TIL-Bs)have a crucial,synergistic role in tumor control.However,little is known about the role TIL-Bs play in immune microenvironment and the way TIL-Bs affect the outcome of immune checkpoint blockade.Using single-cell RNA sequencing(scRNA-seq)data from the Gene Expression Omnibus(GEO)database,the study identified distinct gene expression patterns in TIL-Bs.HNSCC samples were categorized into TIL-Bs inhibition and TIL-Bs activation groups using unsupervised clustering.This classification was further validated with TCGA HNSCC data,correlating with patient prognosis,immune cell infiltration,and response to immunotherapy.We found that the B cells activation group exhibited a better prognosis,higher immune cell infiltration,and distinct immune checkpoint levels,including elevated PD-L1.A prognostic model was also developed and validated,highlighting four genes as potential biomarkers for predicting survival outcomes in HNSCC patients.Overall,this study provides a foundational approach for B cells-based tumor classification in HNSCC,offering insights into targeted treatment and immunotherapy strategies.

Ameloblastoma is a benign tumor characterized by locally invasive phenotypes,leading to facial bone destruction and a high recurrence rate.However,the mechanisms governing tumor initiation and recurrence are poorly understood.Here,we uncovered cellular landscapes and mechanisms that underlie tumor recurrence in ameloblastoma at single-cell resolution.Our results revealed that ameloblastoma exhibits five tumor subpopulations varying with respect to immune response(IR),bone remodeling(BR),tooth development(TD),epithelial development(ED),and cell cycle(CC)signatures.Of note,we found that CC ameloblastoma cells were endowed with stemness and contributed to tumor recurrence,which was dominated by the EZH2-mediated program.Targeting EZH2 effectively eliminated CC ameloblastoma cells and inhibited tumor growth in ameloblastoma patient-derived organoids.These data described the tumor subpopulation and clarified the identity,function,and regulatory mechanism of CC ameloblastoma cells,providing a potential therapeutic target for ameloblastoma.