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TACC3 is an independent prognostic marker, and knockdown of TACC3 enhances the efficacy of CDK1 inhibitor RO3306 in liver cancer cells

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单位: [1]Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. [2]Experimental Medicine Center,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan,China. [3]Department of osteology, Yellow River Central Hospital of the Yellow River Conservancy Commission, Zhengzhou, China. [4]Department of Rheumatology, The Third Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China. [5]Department of Emergency, Henan Province Hospital of Traditional Chinese Medicine, Zhengzhou, Henan Province, China.
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关键词: CDK1 hepatocellular carcinoma mitosis prognosis TACC3

摘要:
The drug resistance of single-target therapy has gradually become an intractable clinical problem. Combination therapy may be an effective treatment to overcome or postpone drug resistance in cancer. Herein, we discussed the synergistic effect of transforming acidic coiled-coil containing protein 3 (TACC3) suppression and cyclin-dependent kinase 1 (CDK1) in hepatocellular carcinoma (HCC). The Cancer Genome Atlas database and bioinformatics methods were implemented to analyze the expression of CDK1 and TACC3, and predict the biological function of TACC3-related genes in HCC. In addition, in vitro experiments, including cell counting kit 8, transwell and flow cytometry were utilized to evaluate cell proliferation, migration, invasion, cell cycle arrest and apoptosis of HCC cells. Our results demonstrated that TACC3 is an unfavorable and independent prognostic factor to predict poor overall survival (OS) in HCC patients. Genetic inhibition of TACC3 exhibited a remarkable antineoplastic activity of HCC cell lines. Bioinformatic prediction proposed that CDK1 may be the main regulator of TACC3-related genes in HCC. In vitro experimental measurements suggested that a combination of si-TACC3 and CDK1 inhibitor synergistically inhibited cell proliferation and migration, and induced G2 cell cycle arrest and apoptosis of HepG2 or MHCC97H cells. In conclusion, our results revealed a prospective dual-target, TACC3 and CDK1, therapeutic strategy to improve the treatment of HCC.© 2023 Wiley Periodicals LLC.

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出版当年[2022]版:
大类 | 4 区 医学
小类 | 3 区 毒理学 4 区 生化与分子生物学
最新[2025]版:
大类 | 3 区 医学
小类 | 3 区 生化与分子生物学 3 区 毒理学
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出版当年[2021]版:
Q2 TOXICOLOGY Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
最新[2023]版:
Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Q2 TOXICOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

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第一作者单位: [1]Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. [*1]Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Rd, Erqi District, Zhengzhou 450052, Henan Province, China.
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通讯机构: [1]Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. [*1]Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Rd, Erqi District, Zhengzhou 450052, Henan Province, China.
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