■近年来,关于骨肉瘤中非SMC凝缩素I复合物G亚基(NCAPG)的报道很少。本研究旨在探讨NCAPG在骨肉瘤中的生物学作用及其潜在的分子机制,并进一步阐明NCAPG在骨肉瘤中异常表达的原因。
■这里,我们通过生物信息学方法,分析NCAPG在肉瘤组织和正常组织中的差异表达,探讨NCAPG表达水平与肉瘤组织分化的关系,包括肿瘤复发,转移,和病人的生存。接下来,通过多个在线网站工具预测骨肉瘤中NCAPG异常表达的转录因子,并通过细胞实验进行验证.随后,进行功能丧失和细胞表型实验以证实NCAPG对骨肉瘤细胞恶性生物学行为的影响。机械上,通过回顾文献,我们发现NCAPG可以通过调节Wnt/β-catenin信号通路影响多种实体肿瘤的恶性进展。因此,我们通过westernblot实验初步研究了NCAPG在骨肉瘤中对该通路的潜在作用。
■与正常组织相比,在肉瘤中发现NCAPG的表达增加,与分化差呈正相关,转移,预后不良。结合转录因子预测结果,相关分析,和TCGA公共数据库中的表达水平,以及体外细胞测定的验证结果,我们发现E2F转录因子1(E2F1)调节骨肉瘤中NCAPG的表达增加。细胞表型实验结果表明沉默NCAPG可以抑制细胞增殖,迁移,和骨肉瘤细胞的侵袭。初步机制研究表明,NCAPG可能通过Wnt/β-catenin途径影响骨肉瘤的进展。
■我们的数据表明,E2F1通过调节NCAPG基因的转录促进骨肉瘤中NCAPG的表达。NCAPG的上调通过Wnt/β-连环蛋白信号轴促进骨肉瘤进展。
UNASSIGNED: In recent years, there are few reports on non-SMC condensin I complex subunit G (NCAPG) in osteosarcoma. Our study aims to explore the biological role of NCAPG in osteosarcoma and its underlying molecular mechanism and to further clarify the reasons for the abnormal expression of NCAPG in osteosarcoma.
UNASSIGNED: Here, we mined The Cancer Genome Atlas (TCGA) Program public database through bioinformatics methods, analyzed the differential expression of NCAPG in sarcoma tissue and normal tissue, and explored the relationship between NCAPG expression level and sarcoma tissue differentiation, including tumor recurrence, metastasis, and patient survival. Next, the transcription factors responsible for the abnormal expression of NCAPG in osteosarcoma tumors were predicted by multiple online website tools and verified via cellular experiments. Subsequently, loss of function and cell phenotype experiments were performed to confirm the effect of NCAPG on the malignant biological behavior of osteosarcoma cells. Mechanistically, by reviewing the literature, we found that NCAPG can affect the malignant progression of many solid tumors by regulating the Wnt/β-catenin signaling pathway. Therefore, we preliminarily investigated the potential effect of NCAPG on this pathway via western blot experiments in osteosarcoma.
UNASSIGNED: Increased expression of NCAPG was found in sarcoma compared to normal tissues, which was positively correlated with poor differentiation, metastasis, and poor prognosis. Combining the transcription factor prediction results, correlation analysis, and expression level in the TCGA public database with validation outcomes of in vitro cell assays, we found that E2F transcription factor 1 (E2F1) regulated the increased expression of NCAPG in osteosarcoma. The results of cell phenotype experiments showed that silencing NCAPG could inhibit the proliferation, migration, and invasion of osteosarcoma cells. The preliminary mechanistic investigation suggested that NCAPG may affect osteosarcoma progression through the Wnt/β-catenin pathway.
UNASSIGNED: Our data reveal that E2F1 facilitates NCAPG expression in osteosarcoma by regulating the transcription of the NCAPG gene. Up-regulation of NCAPG promotes osteosarcoma progression via the Wnt/β-catenin signaling axis.