Identifying Key Genes for Nasopharyngeal Carcinoma by Prioritized Consensus Differentially Expressed Genes Caused by Aberrant Methylation

Chen, Yunqin; Zhou, Chun; Li, Hua-Bin; Li, Hong; Li, Yixue

doi:10.7150/jca.49392

Cited by 16 publications

(13 citation statements)

References 45 publications

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“…GATA6 has been found to be upregulated and function as an oncogene in several forms of HNSCs. 29,30 More relevantly, GATA6 has been found to promote the malignant behaviors of OSCC cells by activating the transcription of fibronectin 1. 14 Gain-and loss-of functions studies then revealed that suppression of GATA6 suppressed the malignant behaviors of the OSCC cells, which were rescued by COL5A1 upregulation.…”

Section: Discussionmentioning

confidence: 99%

LINC00173 blocks GATA6‐mediated transcription of COL5A1 to affect malignant development of oral squamous cell carcinoma

Chen

Zhao

Yang

et al. 2023

J Oral Pathology Medicine

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Background Aberrant expression of collagen type V alpha 1 chain (COL5A1) has been linked to several forms of human cancers. In this work, we focused on the interaction of the LINC00173/GATA binding protein 6 (GATA6)/COL5A1 axis in the malignant property of oral squamous cell carcinoma (OSCC) cells. Methods We analyzed six publicly accessible datasets GSE160042, GSE74530, GSE138206, GSE23558, GSE31853 and GSE146483 to identify aberrantly expressed genes in OSCC. The expression of COL5A1 in OSCC tissues and cell lines was examined by reverse transcription‐quantitative polymerase chain reaction and/or immunohistochemistry. The regulatory mechanism responsible for COL5A1 transcription was predicted via bioinformatics systems, and the interactions of LINC00173, GATA6, and COL5A1 were identified by immunoprecipitation and luciferase assays. Overexpression or downregulation of COL5A1, GATA6, and LINC00173 were induced in OSCC cell lines to determine their roles in the malignant phenotype of the OSCC cells in vitro and in vivo. Results COL5A1 showed elevated expression in OSCC tissues and cells. The COLA51 knockdown suppressed proliferation, migration and invasiveness, apoptosis resistance, and pro‐angiogenic ability of OSCC cells, and it suppressed the growth and dissemination of xenograft tumors in vivo. GATA6 bound to COL5A1 promoter to activate its transcription, whereas LINC00173 bound to GATA6 to block this transcriptional activation. Overexpression of GATA6 or COL5A1 promoted the malignant phenotype of the OSCC cells, which were blocked upon LINC00173 upregulation. Conclusion This work demonstrates that LINC00173 blocks GATA6‐mediated transcription of COL5A1 to affect malignant development of OSCC.

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Section: Discussionmentioning

confidence: 99%

LINC00173 blocks GATA6‐mediated transcription of COL5A1 to affect malignant development of oral squamous cell carcinoma

Chen

Zhao

Yang

et al. 2023

J Oral Pathology Medicine

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“…Overall, we feel confident to propose the extended assertion that a global correlation loss is present in tumor transcriptomes for more than ten cancer types. Very recently, nasopharyngeal carcinoma [ 33 ], an under-studied cancer type, has also been found with overwhelming transcriptional correlation losses. A possible explanation of such a pan-cancer global correlation attenuation may be the increased heterogeneity in tumor tissues.…”

Section: Discussionmentioning

confidence: 99%

Conditional transcriptional relationships may serve as cancer prognostic markers

Wang

Chen

et al. 2021

BMC Med Genomics

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Background While most differential coexpression (DC) methods are bound to quantify a single correlation value for a gene pair across multiple samples, a newly devised approach under the name Correlation by Individual Level Product (CILP) revolutionarily projects the summary correlation value to individual product correlation values for separate samples. CILP greatly widened DC analysis opportunities by allowing integration of non-compromised statistical methods. Methods Here, we performed a study to verify our hypothesis that conditional relationships, i.e., gene pairs of remarkable differential coexpression, may be sought as quantitative prognostic markers for human cancers. Alongside the seeking of prognostic gene links in a pan-cancer setting, we also examined whether a trend of global expression correlation loss appeared in a wide panel of cancer types and revisited the controversial subject of mutual relationship between the DE approach and the DC approach. Results By integrating CILP with classical univariate survival analysis, we identified up to 244 conditional gene links as potential prognostic markers in five cancer types. In particular, five prognostic gene links for kidney renal papillary cell carcinoma tended to condense around cancer gene ESPL1, and the transcriptional synchrony between ESPL1 and PTTG1 tended to be elevated in patients of adverse prognosis. In addition, we extended the observation of global trend of correlation loss in more than ten cancer types and empirically proved DC analysis results were independent of gene differential expression in five cancer types. Conclusions Combining the power of CILP and the classical survival analysis, we successfully fetched conditional transcriptional relationships that conferred prognosis power for five cancer types. Despite a general trend of global correlation loss in tumor transcriptomes, most of these prognosis conditional links demonstrated stronger expression correlation in tumors, and their stronger coexpression was associated with poor survival.

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“…Genetic instability in NPC EBNA1 Disrupts PML NBs (Sivachandran et al, 2008); Upregulates DNMTs and PcG family proteins (Chen et al, 2021b) BALF3 Induce chromosome aberrations and DNA strand breaks (Chiu et al, 2014) LMP1 Represses DDB1-mediated nucleotide excision repair (Chen et al, 2008); impairs Chk1 activation (Deng et al, 2012); upregulates DNMTs (Tsai et al, 2006) miR-BART5-5p, 7-3p, 9-3p, 14-3p modulate ataxia telangiectasia mutated (ATM) gene activity (Lung et al, 2018) Inflammatory response EBERs Enhances TNF-α levels (Li et al, 2015) LMP1…”

Section: Pathogenic Role Of Ebv Viral Products Molecular Mechanismsmentioning

confidence: 99%

The role of Epstein–Barr virus in nasopharyngeal carcinoma

Siak

Leong³

et al. 2023

Front. Microbiol.

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Nasopharyngeal carcinoma (NPC) is a metastasis-prone malignancy closely associated with the Epstein–Barr virus (EBV). Despite ubiquitous infection of EBV worldwide, NPC incidences displayed predominance in certain ethnic groups and endemic regions. The majority of NPC patients are diagnosed with advanced-stage disease, as a result of anatomical isolation and non-specific clinical manifestation. Over the decades, researchers have gained insights into the molecular mechanisms underlying NPC pathogenesis as a result of the interplay of EBV infection with several environmental and genetic factors. EBV-associated biomarkers were also used for mass population screening for the early detection of NPC. EBV and its encoded products also serve as potential targets for the development of therapeutic strategies and tumour-specific drug delivery. This review will discuss the pathogenic role of EBV in NPC and efforts in exploiting the potential of EBV-associated molecules as biomarkers and therapeutic targets. The current knowledge on the role of EBV and its associated products in NPC tumorigenesis, development and progression will offer a new outlook and potential intervention strategy against this EBV-associated malignancy.

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Identifying Key Genes for Nasopharyngeal Carcinoma by Prioritized Consensus Differentially Expressed Genes Caused by Aberrant Methylation

Cited by 16 publications

References 45 publications

LINC00173 blocks GATA6‐mediated transcription of COL5A1 to affect malignant development of oral squamous cell carcinoma

LINC00173 blocks GATA6‐mediated transcription of COL5A1 to affect malignant development of oral squamous cell carcinoma

Conditional transcriptional relationships may serve as cancer prognostic markers

The role of Epstein–Barr virus in nasopharyngeal carcinoma

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