In the present study, the blockade of the Fe-NTA promoted EGFR signaling and sustained ERK activity with β-sitosterol leads to impede tumor promotion and maintenance.Rats which are pre-treated with 20 mg/kg bw of β-sitosterol significantly reduced the elevated expression of p-p38 MAPK, p-JNK, p-ERK, c-fos and c-jun in carcinogen induced rats, which suggest that β-sitosterol might protect renal tissue from neoplastic transformation.
Since STAT3- and JNK-activation are well characterized critical regulators for tumor promotion, the potentiation of their activation in hybrids suggests an additive mechanism enhancing tumor incidence.