Issue 11, 2019

Diallyl trisulfide induces G2/M cell-cycle arrest and apoptosis in anaplastic thyroid carcinoma 8505C cells

Abstract

Anaplastic thyroid cancer (ATC) is the most aggressive thyroid cancer. Current approaches including surgery, chemotherapy and therapeutic drugs provide limited benefits for ATC patients. Diallyl trisulfide (DATS) has been documented as a promising anti-cancer agent for various carcinomas. However, its role in ATC tumorigenesis remained unclear. Our results showed that DATS treatment at 12.5, 25 and 50 μM decreased the viability of 8505C cells both in a time- and dose-dependent manner. The phosphorylation of H2A.X, which is a DNA damage marker, was induced by DATS both in a dose- and time-dependent manner. Moreover, DATS mediated the DNA damage through the phosphorylation of ATM but not ATR. DATS also induced G2/M cell-cycle arrest followed by the translocation of Cdc25C from the nucleus to the cytoplasm. Further results showed that DATS induced mitochondrial apoptosis in 8505C cells, evidenced by Hoechst/PI double staining, PI-Annexin V assay and western blot. Taken altogether, our findings demonstrated that DATS induced G2/M cell-cycle arrest and mitochondrial apoptosis by triggering DNA damage in ATC 8505C cells, which shed light on a novel therapeutic approach for ATC treatment.

Graphical abstract: Diallyl trisulfide induces G2/M cell-cycle arrest and apoptosis in anaplastic thyroid carcinoma 8505C cells

Article information

Article type
Paper
Submitted
28 Mar 2019
Accepted
10 Sep 2019
First published
11 Sep 2019

Food Funct., 2019,10, 7253-7261

Diallyl trisulfide induces G2/M cell-cycle arrest and apoptosis in anaplastic thyroid carcinoma 8505C cells

J. Zheng, X. Cheng, S. Xu, L. Zhang, J. Pan, H. Yu, J. Bao and R. Lu, Food Funct., 2019, 10, 7253 DOI: 10.1039/C9FO00646J

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