PPAR β/δ Agonist GW501516 Inhibits Tumorigenesis and Promotes Apoptosis of the Undifferentiated Nasopharyngeal Carcinoma C666-1 Cells by regulating miR206.

PPARβ/δ Agonist GW501516 Inhibits Tumorigenesis and Promotes Apoptosis of the Undifferentiated Nasopharyngeal Carcinoma C666-1 Cells by regulating miR206. Oncol Res. 2019 Apr 08;: Authors: Ji Y, Li H, Wang F, Gu L Abstract In previous investigations, we reported that peroxisome proliferator-activated receptor β/δ (PPARβ/δ) activation by GW501516 inhibits proliferation and promotes apoptosis in the undifferentiated C666-1 nasopharyngeal carcinoma (NPC) cells by modulating caspase dependent apoptotic pathway. In the present study, the mechanism by which GW501516 induces apoptosis was explored from the perspective of microRNA (miRNA) expression. Among the assayed miRNAs that were involved in regulating the expression of anti-apoptotic protein Bcl-2, miR-206 was increased significantly and specifically by GW501516 in C666-1 cells at both the in-vitro level and at the in-vivo xenograft samples. The induction on miR-206 expression caused by GW501516 was capable of being antagonized by the PPARβ/δ antagonist GSK3787 and AMPK antagonist Dorsomorphin in C666-1 cells. Meanwhile, GW501516's suppression on the growth and apoptosis of C666-1 cells were found to be dependent on the presence of miR-206. MiR-206 overexpression resulted in suppressed proliferation and colony formation ability, and further triggered increased apoptosis in C666-1 cells in a caspase dependent manner. Where the expression of cleaved caspase-3 and caspase-9, and t...
Source: Oncology Research - Category: Cancer & Oncology Tags: Oncol Res Source Type: research