Glioma is one of the most common types of primary intracranial
tumors. The relationship between
triiodothyronine (T3) and
glioma is not clear. This study aimed to investigate the effect of T3 on the proliferation of
glioma cells and its mechanism. Cell viability was analyzed by cell counting kit 8 assay. Flow cytometry analysis was used to detect cell apoptosis and cell cycle.
Thyroid hormone receptor α (THRA) and
thyroid hormone receptor β (THRB) were silenced by transfecting si-THRA and si-THRB plasmids into HS683 and A172
glioma cells. Western blot was performed to assess the
protein expressions. The results indicated that
triiodothyronine (T3) affected the viability, apoptosis and cell cycle of HS683 and A172
glioma cells. Cell apoptosis was significantly inhibited in si-THRA and si-THRB experimental groups. Moreover, knockdown of THRA and THRB reversed the G1 and G2 phase arrest led by T3 and induced an up-regulation of
cyclin D1 expression. The phosphorylated
extracellular signal-regulated kinase (p-ERK), p-AKT, and phosphorylated signal transducer and activator of transcription (p-STAT3)
proteins were markedly increased by inhibiting THRA and THRB in HS683 and A172
glioma cells. T3 affected apoptosis and cell cycle of
glioma cells through regulating THRA and THRB expressions. THRA and THRB may affect
glioma development through regulating, at least partially, the
mitogen-activated protein kinase (MAPK)/ERK and
phosphoinositide 3-kinase (PI3K)/Akt signaling pathways.