MREG suppresses thyroid cancer cell invasion and proliferation by inhibiting Akt-mTOR signaling
MREG suppresses thyroid cancer cell invasion and proliferation by inhibiting Akt-mTOR signaling
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DOI：
10.1016/j.bbrc.2017.07.044
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发表时间：
2017-09-09
影响因子：
3.1
通讯作者：
Pang, Shuguang
中科院分区：
文献类型：
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作者：
Meng, Xiaomei;Dong, Yaozhong;Pang, Shuguang
长期以来，甲状腺癌一直被认为是在中年时期出现的，并在反复增殖后发展为更具侵略性和致命性的癌症。本研究旨在探讨黑素调节蛋白（Melanoregulin，MREG）在甲状腺癌中的生物学功能及其分子机制。结果发现，MREG在甲状腺癌组织中的表达显著下调。MREG表达下调是由表观遗传甲基化引起的。MREG过表达可抑制甲状腺癌细胞的侵袭和增殖。而MREG基因敲减促进甲状腺癌细胞的侵袭和增殖。此外，Akt或mTOR的磷酸化通过MREG过表达而降低，并且通过MREG敲低而增加。此外，Dactolisib（mTOR的抑制剂）可以消除沉默的MREG诱导的甲状腺癌细胞的侵袭和增殖。MREG通过PI3K/Akt-mTOR信号通路调节甲状腺癌细胞的侵袭和增殖。MREG可作为甲状腺癌的一种有前途的治疗策略。(C)2017爱思唯尔公司All rights reserved.
Thyroid cancer has long been considered to arise in middle age and progress to more aggressive and lethal cancers after its repeated proliferation. In this research, we aimed at investigating the biological function and the underlying molecular mechanism of Melanoregulin (MREG) in thyroid cancer. It was found that the expression of MREG was significantly downregulated in thyroid cancer tissues. The downregulation of MREG expression was caused by epigenetic methylation. MREG overexpression could suppress the invasion and proliferation of thyroid cancer cells. While MREG knockdown promoted the invasion and proliferation of thyroid cancer cells. Furthermore, the phosphorylation of Akt or mTOR was decreased by MREG overexpression and increased by MREG knockdown. Moreover, Dactolisib (the inhibitor of mTOR) could abrogate silenced MREG induced thyroid cancer cell invasion and proliferation. Taken together, MREG regulates thyroid cancer cell invasion and proliferation through PI3K/Akt-mTOR signaling pathway. MREG may serve as a promising therapeutic strategy for thyroid cancer. (C) 2017 Elsevier Inc. All rights reserved.