姜黄素通过调控lncRNA LINC00691抑制甲状腺乳头状癌细胞增殖

Zhihua Li, Youbing Gao, Lijun Li, Shanshan Xie
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引用次数: 10

摘要

乳头状甲状腺癌(PTC)是一种上皮来源的分化型甲状腺癌,据报道占甲状腺癌的大多数。姜黄素是一种多酚类化合物,是姜科(生姜)家族的成员,从姜黄植物中提取,具有抗癌作用。在此,我们旨在研究姜黄素对PTC的影响并阐明其机制。因此,姜黄素联合/不联合长链非编码RNA LINC00691抑制PTC B-CPAP细胞,以确定姜黄素在PTC细胞中的作用及其与LINC00691的关系。我们观察到姜黄素治疗降低了B-CPAP细胞的增殖,促进了细胞凋亡。姜黄素抑制B-CPAP细胞中LINC00691的表达。姜黄素单独给药或si-LINC00691单独转染可提高B-CPAP细胞ATP水平,抑制葡萄糖摄取和乳酸水平,抑制乳酸脱氢酶A和己糖激酶2蛋白表达,联合处理可进一步增强。此外,姜黄素或si-LINC00691单独转染可抑制p-Akt活性,联合处理可进一步抑制p-Akt活性。Akt抑制可促进B-CPAP细胞凋亡,抑制Warburg效应。综上所述,我们的研究结果表明姜黄素通过抑制LINC00691促进B-CPAP细胞凋亡,抑制增殖和Warburg效应。其精确的分子机制可能通过Akt信号通路介导,为姜黄素治疗PTC提供理论依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Curcumin Inhibits Papillary Thyroid Cancer Cell Proliferation by Regulating lncRNA LINC00691
Papillary thyroid cancer (PTC) is a type of epithelial-derived differentiated TC that reportedly accounts for a majority of TCs. Curcumin, a polyphenolic compound and a member of the Zingiberaceae (ginger) family derived from turmeric plants, can exhibit anticancer effects. Herein, we aimed to investigate the effect of curcumin on PTC and elucidate underlying mechanisms. Accordingly, PTC B-CPAP cells were treated with curcumin, in combination with/without long noncoding RNA LINC00691 inhibition, to determine the effect of curcumin and its relationship with LINC00691 in PTC cells. We observed that curcumin treatment decreased B-CPAP cell proliferation and promoted apoptosis. Curcumin inhibited LINC00691 expression in B-CPAP cells. Curcumin administration or si-LINC00691 transfection alone promoted ATP levels, inhibited glucose uptake and lactic acid levels, and inhibited lactate dehydrogenase A and hexokinase 2 protein expression in B-CPAP cells, which were further enhanced by combination treatment. Moreover, curcumin administration or si-LINC00691 transfection alone inhibited p-Akt activity, further suppressed by combination treatment. Akt inhibition promoted apoptosis and suppressed the Warburg effect in B-CPAP cells. In conclusion, our findings indicate that curcumin promotes apoptosis and suppresses proliferation and the Warburg effect by inhibiting LINC00691 in B-CPAP cells. The precise molecular mechanism might be mediated through the Akt signaling pathway, providing a theoretical basis for the treatment of PTC with curcumin.
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