Zhao Nan, Ni Chunsheng, Fan Shuai, Che Na, Li Yanlei, Wang Song, Li Yongli, Dong Xueyi, Guo Yuhong, Zhao Xiulan, Liu Tieju
Department of Pathology, Tianjin Medical University, Tianjin 300070, China.
Department of Pathology, General Hospital, Tianjin Medical University, Tianjin 300052, China.
Cancers (Basel). 2023 Dec 19;16(1):15. doi: 10.3390/cancers16010015.
Triple-negative breast cancer (TNBC) has a shorter survival time and higher mortality rate than other molecular subtypes. RSRC2 is a newly discovered tumor suppressor gene. However, the potential functional mechanism of RSRC2 in TNBC remains unknown so far. Multiple bioinformatics databases were used. A Human Transcriptome Array 2.0 analysis, ChIP-seq analysis, ChIP-qPCR, RT-qPCR, Western blot, cell function assays in vitro and a metastatic mouse model in vivo were performed to demonstrate the role of RSRC2 in TNBC. Through the analysis of various databases, RSRC2 expression was the lowest in TNBC tissues compared to other molecular subtypes. The low expression of RSRC2 was associated with a worse prognosis for patients with breast cancer. The transcriptome array, ChIP-seq and bioinformatics analysis identified that GRHL2 and SCIN might have a close relationship with RSRC2. The functional bioinformatics enrichment analysis and functional cell experiments showed that RSRC2 was involved in cell adhesion, cell proliferation, cell migration and invasion. Furthermore, RSRC2 expression suppressed SCIN expression but not GRHL2 expression. SCIN re-expression in the RSRC2 overexpression cells or SCIN knockdown in the RSRC2 knockdown cells reversed the cellular function caused by RSRC2. Mechanistically, RSRC2 transcriptionally inhibited SCIN expression. In summary, our study reveals that RSRC2 acts as a tumor suppressor in TNBC development and progression through negatively regulating SCIN-mediated cell function, thus providing a potential target for TNBC treatment.
三阴性乳腺癌(TNBC)的生存时间比其他分子亚型更短,死亡率更高。RSRC2是一个新发现的肿瘤抑制基因。然而,RSRC2在TNBC中的潜在功能机制目前仍不清楚。本研究使用了多个生物信息学数据库。通过人类转录组芯片2.0分析、ChIP-seq分析、ChIP-qPCR、RT-qPCR、蛋白质免疫印迹、体外细胞功能测定以及体内转移小鼠模型,来证明RSRC2在TNBC中的作用。通过对各种数据库的分析,发现与其他分子亚型相比,RSRC2在TNBC组织中的表达最低。RSRC2的低表达与乳腺癌患者的预后较差相关。转录组芯片、ChIP-seq和生物信息学分析表明,GRHL2和SCIN可能与RSRC2关系密切。功能生物信息学富集分析和功能性细胞实验表明,RSRC2参与细胞黏附、细胞增殖、细胞迁移和侵袭。此外,RSRC2表达抑制SCIN表达,但不抑制GRHL2表达。在RSRC2过表达细胞中重新表达SCIN或在RSRC2敲低细胞中敲低SCIN可逆转由RSRC2引起的细胞功能。机制上,RSRC2转录抑制SCIN表达。总之,我们的研究表明,RSRC2通过负向调节SCIN介导的细胞功能,在TNBC的发生和发展中发挥肿瘤抑制作用,从而为TNBC治疗提供了一个潜在靶点。