Genomic and transcriptional characterization of early esophageal squamous cell carcinoma

Zhao, Jingjing; Jia, Xiya; Li, Qiaojuan; Zhang, He-Na; Wang, Jianjun; Huang, Shenglin; Hu, Zhixiang; Li, Caiping

doi:10.1186/s12920-023-01588-7

Cited by 6 publications

(2 citation statements)

References 47 publications

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“… 36 Third, CCAT1 can serve as a scaffold for two epigenetic modification complexes. 37 Last, CCAT1 acts as a competitive endogenous RNA (ceRNA). 38 However, considering the diversity of lncRNA regulatory mechanisms, the functional role of CCAT1 and its mechanism in tumorigenesis promoted by bacterial infection remain to be determined.…”

Section: Introductionmentioning

confidence: 99%

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Persistent infection with Porphyromonas gingivalis increases the tumorigenic potential of human immortalised oral epithelial cells through ZFP36 inhibition

Lu,

Cao,

Geng

et al. 2024

Cell Proliferation

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The association between Porphyromonas gingivalis infection and oral squamous cell carcinoma (OSCC) has been established by numerous epidemiological studies. However, the underlying mechanism specific to this connection remains unclear. By bioinformatical analysis, we identified ZFP36 as a potentially significant co‐expressed gene in both the OSCC gene database and the persistent infection model of P. gingivalis. To further investigate the role of ZFP36, we established a cell model that human immortalized oral epithelial cells (HIOECs) that were sustainedly infected by P. gingivalis (MOI = 1) for a duration of 30 weeks. Our findings indicated that sustained infection with P. gingivalis inhibited the expression of ZFP36 protein and induced changes in the biological behaviour of HIOECs. The mechanism investigation demonstrated the potential role of ZFP36 in regulating the cancer‐related biological behaviour of HIOECs. Subsequent studies revealed that highly expressed CCAT1 could serve as a molecular scaffold in the formation of the ZFP36/CCAT1/MK2 complex. This complex formation enhanced the binding abundance of MK2 and ZFP36, thereby promoting the inhibition of ZFP36 protein phosphorylation. To summarize, low expression of ZFP36 protein under persistent P. gingivalis infection enhances the cancer‐related biological behaviour of HIOECs.

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Section: Introductionmentioning

confidence: 99%

“…Second, CCAT1 forms DNA/RNA/protein complexes that regulate protein enhancer activity 36 . Third, CCAT1 can serve as a scaffold for two epigenetic modification complexes 37 . Last, CCAT1 acts as a competitive endogenous RNA (ceRNA) 38 .…”

Section: Introductionmentioning

confidence: 99%

Persistent infection with Porphyromonas gingivalis increases the tumorigenic potential of human immortalised oral epithelial cells through ZFP36 inhibition

Lu,

Cao,

Geng

et al. 2024

Cell Proliferation

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Multimodal analysis of cfDNA methylomes for early detecting esophageal squamous cell carcinoma and precancerous lesions

Liu,

Dai,

Wang

et al. 2024

Nat Commun

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Detecting early-stage esophageal squamous cell carcinoma (ESCC) and precancerous lesions is critical for improving survival. Here, we conduct whole-genome bisulfite sequencing (WGBS) on 460 cfDNA samples from patients with non-metastatic ESCC or precancerous lesions and matched healthy controls. We develop an expanded multimodal analysis (EMMA) framework to simultaneously identify cfDNA methylation, copy number variants (CNVs), and fragmentation markers in cfDNA WGBS data. cfDNA methylation markers are the earliest and most sensitive, detectable in 70% of ESCCs and 50% of precancerous lesions, and associated with molecular subtypes and tumor microenvironments. CNVs and fragmentation features show high specificity but are linked to late-stage disease. EMMA significantly improves detection rates, increasing AUCs from 0.90 to 0.99, and detects 87% of ESCCs and 62% of precancerous lesions with >95% specificity in validation cohorts. Our findings demonstrate the potential of multimodal analysis of cfDNA methylome for early detection and monitoring of molecular characteristics in ESCC.

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FADD amplification is associated with CD8⁺ T‐cell exclusion and malignant progression in HNSCC

Zheng,

Sheng,

et al. 2024

Oral Diseases

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ObjectiveThis study aimed to clarify the relationship between FADD amplification and overexpression and the tumor immune microenvironment.MethodsImmunohistochemical staining and bioanalysis were used to analyze the association between FADD expression in tumor cells and cells in tumor microenvironment. RNA‐seq analysis was used to detect the differences in gene expression upon FADD overexpression. Flow cytometry and multicolor immunofluorescence staining (mIHC) were used to detect the differences in CD8+ T‐cell infiltration in FADD‐overexpressed cells or tumor tissues.ResultsOverexpression of FADD significantly promoted tumor growth. Cells with high FADD expression presented high expression of CD276 and FGFBP1 and low expression of proinflammatory factors (such as IFIT1‐3 and CXCL8), which reduced the percentage of CD8+ T cells and created a “cold tumor” immune microenvironment, thus promoting tumor progression. In vivo and in vitro experiment confirmed that tumor tissues with excessive FADD expression exhibited CD8+ T‐cell exclusion in the microenvironment.ConclusionOur preliminary investigation has discovered the association between FADD expression and the immunosuppressive microenvironment in HNSCC. Due to the high frequent amplification of the chromosomal region 11q13.3, where FADD is located, targeting FADD holds promise for improving the immune‐inactive state of tumors, subsequently inhibiting HNSCC tumor progression.

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Genomic and transcriptional characterization of early esophageal squamous cell carcinoma

Cited by 6 publications

References 47 publications

Persistent infection with Porphyromonas gingivalis increases the tumorigenic potential of human immortalised oral epithelial cells through ZFP36 inhibition

Persistent infection with Porphyromonas gingivalis increases the tumorigenic potential of human immortalised oral epithelial cells through ZFP36 inhibition

Multimodal analysis of cfDNA methylomes for early detecting esophageal squamous cell carcinoma and precancerous lesions

FADD amplification is associated with CD8⁺ T‐cell exclusion and malignant progression in HNSCC

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Genomic and transcriptional characterization of early esophageal squamous cell carcinoma

Cited by 6 publications

References 47 publications

Persistent infection with Porphyromonas gingivalis increases the tumorigenic potential of human immortalised oral epithelial cells through ZFP36 inhibition

Persistent infection with Porphyromonas gingivalis increases the tumorigenic potential of human immortalised oral epithelial cells through ZFP36 inhibition

Multimodal analysis of cfDNA methylomes for early detecting esophageal squamous cell carcinoma and precancerous lesions

FADD amplification is associated with CD8+ T‐cell exclusion and malignant progression in HNSCC

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FADD amplification is associated with CD8⁺ T‐cell exclusion and malignant progression in HNSCC