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Synergic radiosensitization of sinomenine hydrochloride and radioiodine on human papillary thyroid carcinoma cells.

ABSTRACT: Radioiodine (¹³¹I) therapy is an important treatment for thyroid carcinoma. The response to radiotherapy sometimes limited by the development of radioresistance. Sinomenine hydrochloride(SH), was reported as a prospective radiosensitizer. This study was aim to evaluate synergic radiosensitization of SH and ¹³¹I on papillary thyroid carcinoma (PTC). We evaluated HTori-3, BCPAP and TPC-1 cells, the cell viability was evaluated by MTT. The experiment was divided into 4 groups: control group, SH (0.8 mM) group, I (¹³¹I 14.8 MBq/ml) group and ISH (SH 0.8 mM plus ¹³¹I 14.8 MBq/ml) group. Flow cytometry was used to investigate cell cycle phases and cell apoptosis. RT-PCR and western blotting were performed to determine the molecular changes. Compared to control group, SH significantly increased apoptosis and enhanced radiosensitivity of HTori-3 and PTC cells were related to the ratio of Bcl-2 to Bax protein downregulation and Fas, p21, p-ATM, p-Chk1, p-Chk2 and p53 protein expression upregulation in the ISH group (P < 0.05). Our results indicate that synergic radiosensitization of SH and iodine-131 on PTC cells and SH could be a potential therapeutic radiosensitizer in PTC radio therapy after total thyroidectomy.

SUBMITTER: Zhao A

PROVIDER: S-EPMC8273215 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundPapillary thyroid cancer (PTC) is the most frequent endocrine tumor. Radioiodine (RAI) treatment is highly effective in these tumors, but up to 60% of metastatic cases become RAI-refractory. Scanty data are available on either the molecular pattern of radioiodine refractory papillary thyroid cancers (PTC) or the mechanisms responsible for RAI resistance.MethodsWe analyzed the molecular profile and gene/miRNA expression in primary PTCs, synchronous and RAI-refractory lymph node metastases (LNMs) in correlation to RAI avidity or refractoriness. We classified patients as RAI+/D+ (RAI uptake/disease persistence), RAI-/D+ (absent RAI uptake/disease persistence), and RAI+/D- (RAI uptake/disease remission), and analyzed the molecular and gene/miRNA profiles, and the expression of thyroid differentiation (TD) related genes.ResultsA different molecular profile according to the RAI class was observed: BRAFV600E cases were more frequent in RAI-/D+ (P = 0.032), and fusion genes in RAI+/D+ cases. RAI+/D- patients were less frequently pTERT mutations positive, and more frequently wild type for the tested mutations/fusions. Expression profiles clearly distinguished PTC from normal thyroid. On the other hand, in refractory cases (RAI+/D+ and RAI-/D+) no distinctive PTC expression patterns were associated with either tissue type, or RAI uptake, but with the driving lesion and BRAF-/RAS-like subtype. Primary tumors and RAI-refractory LNMs with BRAFV600E mutation display transcriptome similarity suggesting that RAI minimally affects the expression profiles of RAI-refractory metastases. Molecular profiles associated with the expression of TPO, SLC26A4 and TD genes, that were found more downregulated in BRAFV600E than in gene fusions tumors.ConclusionsThe present data indicate a different molecular profile in RAI-avid and RAI-refractory metastatic PTCs. Moreover, BRAFV600E tumors displayed reduced differentiation and intrinsic RAI refractoriness, while PTCs with fusion oncogenes are RAI-avid but persistent, suggesting different oncogene-driven mechanisms leading to RAI refractoriness.

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Synergic radiosensitization of sinomenine hydrochloride and radioiodine on human papillary thyroid carcinoma cells.

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