A biomarker and molecular mechanism investigation for thyroid cancer

Abstract

Introduction:This study aimed to reveal the potential molecular mechanism associated with thyroid cancer (THCA) prognosis, and investigate promising biomarkers for THCA.Material and methods: Differentially expressed genes (DEGs) were compared between THCA samples (THCA group) and normal samples (N group). Then, enrichment analysis and protein-protein interaction (PPI) network analysis were performed, followed by prognostic hub gene exploration from the PPI network. Furthermore, the prognostic and mutation analysis was performed on these hub genes. Finally, the associations of the hub gene with immune cells were investigated.Results: A total of 802 DEGs were obtained between the THCA group and the N group. These DEGs were mainly enriched in pathways such as lysine degradation. From the PPI network, 20 hub genes, including CD44, CCND1, SNAI1, and KIT, were investigated. The survival analysis showed that the up-regulation of CD44 and down-regulation of SNAI1 contributed to the favorable and unfavorable outcomes of patients with THCA, respectively. Meanwhile, the diagnostic analysis showed that the AUC of KIT in THCA was larger than 0.9. Furthermore, the gene mutation analysis showed that the alternated CCND1 participated in the cell cycle pathway. Finally, the correlation analysis showed that prognostic genes such as CD44 were positively correlated with immune cells such as M1 macrophages.Conclusions: A total of 20 hub genes including CCND1, CD44, SNAI1, and KIT were revealed as potential biomarkers for the differential diagnosis, prognosis, and development of drug targets of THCA. The lysine degradation pathway and cell cycle pathway might take part in the progression of THCA.

Papillary Thyroid Cancer Remodels the Genetic Information Processing Pathways

“…Figure 4 justifies the increased proliferation of the cancer cells through up-regulated CCND1 (x (T) = 3.48; x (Φ) = 4.78; x (Θ) = 8.85), one of the 20 hub genes used as a biomarker for thyroid cancer [107]. Survival of the cancer cells is optimized through the up-regulation of several key genes, ensuring evading apoptosis such are BIRC5 (x (T) = 6.04) and DDB2 (x (T) = 2.37).…”

Papillary Thyroid Cancer Remodels the Genomic Fabrics of DNA Replication, Repair and Transcription

“…Figure 4 justifies the increased proliferation of the cancer cells through up-regulated CCND1 (x (T) = 3.48; x (Φ) = 4.78; x (Θ) = 8.85), one of the 20 hub genes used as biomarker for the thyroid cancer [92]. Survival of the cancer cells is optimized through the up-regulation of several key genes ensuring evading apoptosis such are BIRC5 (x (T) = 6.04) and DDB2 (x (T) = 2.37).…”

Advances in targeted therapy and biomarker research in thyroid cancer

“…Promoting the start of long-term follow-up studies to better understand post-treatment survival outcomes and the quality of life of thyroid cancer patients. (7) Patient education and engagement. Emphasizing the necessity of patient education about the advantages and potential negative effects of targeted therapy, as well as the value of biomarker testing.…”

“…Thyroid cancer molecular biomarker research has made great progress, providing important insights into the disease’s complexity ( 7 ). Proteomics and genomics advances have revealed particular genetic abnormalities and molecular changes linked to distinct subtypes of thyroid cancer ( 7 ). Markers such as BRAF and RAS mutations have become critical for diagnosis and prognosis ( 8 , 9 ).…”

“…Molecular biomarkers are essential for thyroid cancer diagnosis, prognosis, and treatment because they offer important information on the molecular features of the illness ( 7 ). BRAF mutation ( 8 ), RAS mutation ( 9 ), RET/PTC rearrangement ( 10 ), PAX8/PPARγ rearrangement ( 11 ), and TERT promoter mutation ( 12 ), are among the major molecular indicators linked to thyroid cancer.…”