Open AccessMulberry anthocyanins improves thyroid cancer progression mainly by inducing apoptosis and autophagy cell death
Author(s) -
Long HouLong,
Zhang FengFeng,
Wang HongLing,
Yang WenShi,
Hou HaiTao,
Yu JingKui,
Liu Bin
Publication year - 2018
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2017.11.004
Subject(s) - medicine , autophagy , apoptosis , thyroid cancer , programmed cell death , cancer research , cancer , thyroid , oncology , genetics , biology
Dietary anthocyanin compounds have multiple biological effects, including antioxidant, anti‐inflammatory, and anti‐atherosclerotic characteristics. The present study evaluated the anti‐tumor capacity of mulberry anthocyanins (MA) in thyroid cancer cells. Our data showed that MA suppressed SW1736 and HTh‐7 cell proliferation in a time‐ and dose‐dependent manner. Meanwhile, flow cytometry results indicated that MA significantly increased SW1736 and HTh‐7 cell apoptosis. We additionally observed that SW1736 and HTh‐7 cell autophagy was markedly enhanced after MA treatment. Importantly, anthocyanin‐induced cell death was largely abolished by 3‐methyladenine (3‐MA) or chloroquine diphosphate salt (CQ) treatment, suggesting that MA‐induced SW1736 and HTh‐7 cell death was partially dependent on autophagy. In addition, activation of protein kinase B (Akt), mammalian target of rapamycin (mTOR), and ribosomal protein S6 (S6) were significantly suppressed by anthocyanin exposure. In summary, MA may serve as an adjunctive therapy for thyroid cancer patients through induction of apoptosis and autophagy‐dependent cell death.