SLC27A6 (Solute Carrier Family 27 Member 6)

Our research successfully identified six hub genes in CRC through a series of rigorous analyses and experimental validations. These findings provide important molecular basis for further investigation into the pathogenesis and progression of CRC.

Lipid metabolism dysregulation plays a crucial role in the progression of OLP to OSCC. Targeting key lipid metabolism pathways and genes, such as DAG, TAG, PI, and the PPAR pathway, may offer promising strategies for early diagnosis and therapeutic intervention. This study provides novel insights into the molecular mechanisms of OLP-to-OSCC progression and suggests potential drug candidates, including natural compounds, for future clinical applications. Further research is needed to validate these findings in clinical settings.

The transcription level of the CCL20 and CDKN2A genes becomes increased at the stage of neoplastic epithelial changes and stays so in cervical cancer. Validation on an independent microarray dataset showed that the differential expression patterns of the CDKN2A and SLC27A6 genes were conserved in the respective gene expression comparisons between groups.

In comparison to healthy brain tissue, glioblastoma tumors take up fewer fatty acids. The metabolism of fatty acids in glioblastoma is dependent on factors such as obesity and smoking.

Our results suggested that these identified genes with prognostic features were regulated by DNA methylation of their promoters. Our studies demonstrated the potential application of DNA methylation markers in the prognosis of LUAD.

Knockdown of SLC27A6 inhibited c-MYC expression. Our results suggest that SLC27A6 is overexpressed in PTC tissues and affects the progression of PTC by regulating c-MYC.

Furthermore, re-expression of SLC27A6 inhibited the growth capacity of NPC cells but strengthened the CSC markers. Our findings revealed the dual role of SLC27A6 in NPC and shed novel light on the link between lipid metabolism and CSC maintenance.