Dokumentdetails
ID

doi:10.1038/s41419-023-05709-z...

Autor
Jingtai, Zhi Linfei, Hu Yuyang, Qian Ning, Kang Xinwei, Yun Xin, Wang Xianhui, Ruan Dongmei, Huang Weiwei, Yang Xiangrui, Meng Tianze, Zhu Wei, Wang Xiangqian, Zheng
Langue
en
Editor

Nature

Kategorie

Life Sciences

Jahr

2023

Auflistungsdatum

05.04.2023

Schlüsselwörter
sorafenib carcinoma pfkfb3-mediated glycolysis supply tc effect aurora-a thyroid
Metrisch

Zusammenfassung

Thyroid cancer (TC) is the most common endocrine tumor, amongst which anaplastic thyroid carcinoma (ATC) is the most deadly.

Aurora-A usually functions as oncogenes, and its inhibitor Alisertib exerts a powerful antitumor effect in various tumors.

However, the mechanism of Aurora-A in regulating TC cell energy supply remains unclear.

In the present study, we demonstrated the antitumor effect of Alisertib and an association between high Aurora-A expression and shorter survival.

Multi-omics data and in vitro validation data suggested that Aurora-A induced PFKFB3-mediated glycolysis to increase ATP supply, which significantly upregulated the phosphorylation of ERK and AKT.

Furthermore, the combination of Alisertib and Sorafenib had a synergistic effect, further confirmed in xenograft models and in vitro.

Collectively, our study provides compelling evidence of the prognostic value of Aurora-A expression and suggests that Aurora-A upregulates PFKFB3-mediated glycolysis to enhance ATP supply and promote TC progression.

Combining Alisertib with Sorafenib has huge prospects for application in treating advanced thyroid carcinoma.

Jingtai, Zhi,Linfei, Hu,Yuyang, Qian,Ning, Kang,Xinwei, Yun,Xin, Wang,Xianhui, Ruan,Dongmei, Huang,Weiwei, Yang,Xiangrui, Meng,Tianze, Zhu,Wei, Wang,Xiangqian, Zheng, 2023, Targeting Aurora-A inhibits tumor progression and sensitizes thyroid carcinoma to Sorafenib by decreasing PFKFB3-mediated glycolysis, Nature

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