Analysis of CLDN۱ Gene Expression in Colorectal Cancer: Role in Tight Junctions and Tumor Progression
- سال انتشار: 1403
- محل انتشار: دومین کنگره بین المللی کنسرژنومیکس
- کد COI اختصاصی: ICGCS02_035
- زبان مقاله: انگلیسی
- تعداد مشاهده: 148
نویسندگان
Shahid Ashrafi Isfahani University
Yazd University
Yazd University
Azad University
چکیده
Claudin-۱ (CLDN۱) is a tight junction protein that plays a vital role in maintaining epithelial cell polarity and barrier function. Dysregulation of CLDN۱ expression has been implicated in the progression of several cancers, including colorectal cancer. In this study, we aim to analyze the expression levels of the CLDN۱ gene in colorectal cancer tissues using microarray data. CLDN۱ is known to interact with several key genes such as TJP۱, GRB۷, FERMT۱, SH۳RF۲, LAMC۲, SOX۹, SEMA۳F, RHOD, EGFR, BCAR۱, and EPHA۲, which are involved in critical signaling pathways. Additionally, a single nucleotide polymorphism (SNP), rs۱۴۰۸۴۶۶۲۹, is associated with mutations in the CLDN۱ gene. The CLDN۱ protein interacts most strongly with OCLN, and it is involved in the KEGG tight junction signaling pathway, playing a significant role in cancer progression. Methods: Microarray data for colorectal cancer samples were obtained from public databases, and the expression levels of the CLDN۱ gene were analyzed. The analysis was performed using standard bioinformatics tools for normalization, differential gene expression analysis, and pathway enrichment. Gene interaction networks were constructed to identify the genes with which CLDN۱ interacts most significantly, with a focus on genes involved in tight junction formation and cancer-related signaling pathways. The SNP rs۱۴۰۸۴۶۶۲۹ was also investigated to understand its potential impact on CLDN۱ function. Protein interaction analysis was conducted, highlighting the interaction between CLDN۱ and OCLN, which is crucial for maintaining cell adhesion in epithelial tissues. Results: The microarray analysis revealed a significant overexpression of the CLDN۱ gene in colorectal cancer tissues compared to normal tissues. This upregulation of CLDN۱ was closely linked with tumor aggressiveness and invasion, suggesting that the gene plays a role in promoting malignancy. The interaction network analysis showed that CLDN۱ had the strongest interactions with TJP۱ and OCLN, both of which are integral components of the tight junction signaling pathway. Other interacting genes such as EGFR and SOX۹ were also highlighted, indicating their potential roles in tumor proliferation and metastasis. The presence of the SNP rs۱۴۰۸۴۶۶۲۹ was associated with alterations in the expression levels of CLDN۱, potentially leading to structural changes in the protein that affect its ability to form tight junctions. The interaction between CLDN۱ and OCLN was shown to be essential for maintaining epithelial barrier integrity, and disruption of this interaction may facilitate cancer cell invasion and spread. These findings suggest that CLDN۱ dysregulation could play a key role in colorectal cancer progression through its impact on cell adhesion and signaling pathways. Conclusion: This study demonstrates that CLDN۱ is significantly overexpressed in colorectal cancer and plays a critical role in tight junction integrity and cancer progression. The SNP rs۱۴۰۸۴۶۶۲۹ may contribute to functional changes in the CLDN۱ protein, further promoting malignancy. The interaction between CLDN۱ and OCLN, as well as other key genes in the tight junction and cancer-related pathways, underscores the importance of CLDN۱ in colorectal cancer biology. Future research may focus on targeting CLDN۱ and its interactions as a therapeutic approach to inhibit cancer progression.کلیدواژه ها
CLDN۱,Colorectal cancer,Tight junctionsمقالات مرتبط جدید
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