Thus, this study investigated the expression of anti-apoptotic B-cell lymphoma 2 (BCL-2) family members, which are frequently overexpressed in many human cancers to inhibit apoptosis, in PTC harboring the BRAF<sup>V600E</sup> mutation after BRAFi treatment, and then evaluated the cytotoxic effects of a homology 3 domain (BH3)-mimetic in combination with a BRAFi.
BH3-profiling of seven fresh primary papillary thyroid cancer (PTC) tumors showed dependence for survival on Bcl-xL (2/7), Bcl2 (2/7), and Mcl-1 (2/7), while the majority of thyroid cell lines were mainly dependent on Bcl-xL.
Remarkably, just like the PTC cancer and NME cells 33.3% of HT and 50% of GD patients' revealed simultaneous "overexpression" of Bcl-2 and 8-OHdG in epithelial cells.
In conclusion, this study documented down-regulation of galectin-3 and Bcl-2 (antiapoptotic molecules) and stepwise increase of survivin (inhibitor of apoptosis), during thyroid tumor progression from PTC to ATC.