Published online Apr 15, 2024. doi: 10.4251/wjgo.v16.i4.1500
Peer-review started: November 21, 2023
First decision: December 27, 2023
Revised: January 7, 2024
Accepted: February 4, 2024
Article in press: February 4, 2024
Published online: April 15, 2024
Processing time: 141 Days and 12.4 Hours
Precancerous lesions including low-grade intraepithelial neoplasia (LGIN) and high-grade IN (HGIN) are a mandatory stage in the development of esophageal squamous cell carcinoma (ESCC). The regulatory molecules driving esophageal carcinogenesis remain unclear, which largely hampers early esophageal cancer diagnosis and treatment.
We aimed to establish a mouse model mimicking the multi-stage development of ESCC and then to examine the key genes involved in the development of ESCC through transcriptome sequencing. Besides, we aimed to explore the immune cell infiltration in the microenvironment associated with the multi-stage progression of ESCC. Additionally, we hope to validate our results using human samples, which may provide a novel perspective for clinical application.
To examine the genes and immune cell infiltration in the microenvironment associated with the multi-stage progression of ESCC to facilitate diagnosis and early intervention.
The mouse model of esophageal tumorigenesis was established by providing 4-nitroquinoline 1-oxide (4NQO) containing water to C57BL/6 mice. The transcriptome sequencing was performed for esophageal tissues with different pathological statuses. Differentially expressed gene analysis (DEGA) and Venn diagram were used to identify key genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were used to explore the biological function of genes. The CIBERSORT algorithm was used to detect the pattern of immune cell infiltration. The immunohistochemistry (IHC) was conducted to validate our results. Furthermore, the Luminex multiplex cytokines analysis was utilized to measure the serum level of cytokines in mice.
A total of 86 genes were identified as key genes in the development of ESCC. Enrichment analysis showed that these genes were mainly enriched in keratinization, epidermal cell differentiation, and interleukin (IL)-17 signaling pathways. CIBERSORT analysis showed that the esophageal carcinogenesis group had more infiltration of M0 and M1 macrophages which was then validated by IHC. Serum cytokines analysis showed that IL-1β and IL-6 were upregulated, while IL-10 was downregulated in LGIN, HGIN, and carcinoma groups. Moreover, the expression of the representative key genes, like S100a8 and Krt6b, was verified in external human samples, and the results of immunohistochemical staining were consistent with the findings in mice.
We identified a set of key genes represented by S100a8 and Krt6b and investigated their potential biological functions. In addition, we found that macrophage infiltration and abnormal alterations of inflammation-associated cytokines, such as IL-1β, IL-6, and IL-10, in the peripheral blood may be closely associated with the development of ESCC.
We have identified a set of key genes that are closely associated with esophageal carcinogenesis and may serve as novel biomarkers for early detection of ESCC. Additionally, the aberrant infiltration of inflammatory macrophages and dysregulation of cytokines may contribute to esophageal carcinogenesis.