关键词: Breast cancer SOX13 TRIM11 glycolysis wnt/β-catenin signaling pathway

Mesh : Animals Autoantigens / metabolism Breast Neoplasms / genetics pathology Cell Line, Tumor Cell Proliferation / genetics Female Glycolysis / genetics Humans Mice Mice, Nude SOXD Transcription Factors / metabolism Tripartite Motif Proteins / metabolism Ubiquitin-Protein Ligases / metabolism Wnt Signaling Pathway / genetics

来  源:   DOI:10.1080/21655979.2022.2073127

Abstract:
Breast cancer is the most frequent cancer among women and the second highest mortality in female across the world. Recent studies have illustrated that sex-determining region Y (SRY)-box protein (SOX) family plays essential roles in regulating various cancers. Nevertheless, the detailed effects of SOX13 on breast cancer are still uncovered. In our present study, SOX13 protein level was measured by using western blot assay in tissues and cells, and the results showed that SOX13 was upregulated in breast cancer tissues and cells compared with normal samples. Moreover, silencing SOX13 inhibited breast cancer cell viability, arrested cell cycle at G1/S phase and suppressed glycolysis, while overexpression of SOX13 reversed these events. Additionally, SOX13 knockdown reduced the level of proteins related to Wnt/β-catenin signaling pathway, whereas overexpression of tripartite motif containing 11 (TRM11) efficiently attenuated the effects, indicating that SOX13 controlled Wnt/β-catenin pathway depending on TRIM11. Furthermore, the data gained from xenograft tumor model illustrated that silencing SOX13 suppressed the tumor growth in nude mice and the glycolysis of tissues. In conclusion, our investigation illustrated that SOX13 facilitated breast cancer cell proliferation and glycolysis by modulating Wnt/β-catenin signaling pathway affected via TRIM11.
摘要:
乳腺癌是女性中最常见的癌症,也是全球女性死亡率第二高的癌症。最近的研究表明,性别决定区Y(SRY)盒蛋白(SOX)家族在调节各种癌症中起着至关重要的作用。然而,SOX13对乳腺癌的详细影响仍未被发现。在我们目前的研究中,SOX13蛋白水平通过使用蛋白质印迹测定法在组织和细胞中测量,结果表明,与正常样本相比,SOX13在乳腺癌组织和细胞中表达上调。此外,沉默SOX13抑制乳腺癌细胞活力,细胞周期阻滞在G1/S期,糖酵解被抑制,而SOX13的过表达逆转了这些事件。此外,SOX13敲低可降低Wnt/β-catenin信号通路相关蛋白水平,而过表达含有11(TRM11)的三方基序有效地减弱了作用,表明SOX13依赖于TRIM11控制Wnt/β-catenin途径。此外,从异种移植肿瘤模型获得的数据表明,沉默SOX13抑制裸鼠的肿瘤生长和组织的糖酵解。总之,我们的研究表明,SOX13通过调节经TRIM11影响的Wnt/β-catenin信号通路促进乳腺癌细胞增殖和糖酵解。
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