TY  - JOUR
TI  - Inhibitory effect of vemurafenib combined with panobinostat on human anaplastic thyroid cancer cells
AU  - Li, Yang
AU  - Gao, Han
AU  - Zhang, Peng
AU  - Wang, Wenjun
AU  - Zhou, Jianwen
AU  - Cui, Jing
AU  - Xue, Di
AU  - Zhang, Baofeng
AU  - Li, Peihong
AU  - Fan, Li
AU  - Xu, Jingwei
JO  - Pakistan Journal of Pharmaceutical Sciences
JA  - Pak. J. Pharm. Sci.
VL  - 39
IS  - 5
SP  - 1556
EP  - 1567
PY  - 2026
DA  - 2026/05
KW  - Anaplastic thyroid cancer cells
KW  - GLUT1
KW  - NIS
KW  - Panobinostat
KW  - Vemurafenib
DO  - 10.36721/PJPS.2026.39.5.REG.13646.1
AB  - Background: Anaplastic thyroid cancer (ATC) is a highly aggressive malignancy with poor prognosis and limited therapeutic options, highlighting the need for novel treatment strategies. Objectives: This study investigated the inhibitory effects of vemurafenib combined with panobinostat on human ATC cell lines (FRO and ARO) and explored the underlying mechanisms. Methods: Four experimental groups were established: Control, vemurafenib (Ve), panobinostat (Pa), and combination treatment (Ve+Pa). Cell proliferation and drug synergy were evaluated using CCK-8 assay, colony formation assay and CompuSyn software. Cell migration, invasion, apoptosis and glucose consumption were assessed using Transwell assays, wound healing assays, apoptosis assays and glucose consumption assays. Molecular markers were examined by RT-qPCR, Western blotting and immunofluorescence. Results: CompuSyn analysis confirmed a synergistic inhibitory effect of Ve+Pa on FRO and ARO cells. The combination treatment significantly suppressed cell proliferation, migration, invasion and glucose consumption while promoting apoptosis compared with single treatments or control. Additionally, expression of the sodium iodide symporter (NIS) and iodine metabolism-related molecules increased, whereas glucose transporter 1 (GLUT1) expression decreased. Conclusion: Vemurafenib combined with panobinostat exerts a synergistic inhibitory effect on the growth and metastasis of ATC cells, enhances apoptosis and promotes cellular redifferentiation, suggesting potential as a therapeutic strategy for anaplastic thyroid cancer.
ER  -