In summary, the results indicate that activation of the COX-2-PGE2 pathway in RCC leads to the development of sunitinib resistance and may serve an important role in the maintenance of the characteristics of stem cells that are closely associated with drug resistance.
The isolated compound HEG can impart momentous chemo-protection against experimental RCC by suppressing the cyclooxygenase (COX-2) and prostaglandin E2 (PGE<sub>2</sub>) expression via nuclear factor-kappa B (NF-κB) pathway.
RCC tissue chips were subjected to IHC staining, which showed COX-2 expression in RCC tissues to be a significantly closely correlated with NOV expression, with significance determined using Pearson correlation testing (P < 0.05).
COX-2 overexpression within these intracellular organelles in RCC may be associated with renal cell carcinogenesis and COX-2 may be a useful biomarker in RCC.
These results demonstrate that the generated COX-2 in human renal cell carcinoma plays an important role in the proliferation of malignant renal cells.