Effect of sinomenine hydrochloride on papillary thyroid carcinoma cell when treated by radioiodine

Introduction: Radioiodine(¹³¹I) therapy is one of the most important treatments for differentiated thyroid carcinoma, however, the response to radiotherapy is sometimes limited by the development of radioresistance. Sinomenine hydrochloride (SH) has anticancer activity. Some studies suggest that SH appears to be a prospective radiosensitizer in cervical cancer & esophageal squamous cell carcinoma therapy. Its effect on BCPAP & TPC1 is unclear at present.

Objectives: We determined the effect of SH on the radiosensitivity of BCPAP & TPC1 cells. BCPAP & TPC1 cells were subjected to SH & ¹³¹I, both separately & in combination. Untreated cells served as controls.

Methods: The MTT assay was used to evaluate cell proliferation. Flow cytometry was used to investigate cell cycle phases & cell apoptosis. Bcl‑2, Bax, TP53 & Fas expression was evaluated using western blotting, the mRNA expression levels of Fas, TP53, Bcl-2 & Bax were analyzed using reverse transcription‑quantitative polymerase chain reaction to different groups.

Results: SH combined with ¹³¹I significantly increased BCPAP & TPC1 cell apoptosis. The molecular mechanism by which SH enhanced radiosensitivity of BCPAP & TPC1 cells was related to Bcl-2 protein downregulation & fas, TP53 & Bax protein expression upregulation. When comparing the only ¹³¹I group with SH combined with ¹³¹I group, we found that In BCPAP the mRNA expression levels of TP53 (6.89, vs. 9.55, respectively; P<0.05) , FAS(2,67 vs. 6.41, respectively; P<0.01), Bcl-2(1.33 vs. 2.92, respectively; P<0.01); in TPC1 the mRNA expression levels of Fas (2.81 vs. 3.14, respectively; P<0.01), the mRNA expression levels of Bax, Bcl-2 & TP53 were negative. SH appears can increase radiosensitivity & improve efficacy of Radioiodine(¹³¹I) therapy for papillary thyroid carcinoma.