PDF(Pubmed)
Abstract：
UNASSIGNED: CSMD2 has been reported as a potential prognostic factor in several cancers. However, whether CSMD2 affects bladder cancer (BC) remains unclear.
UNASSIGNED: Public data were obtained from the TCGA (https://cancergenome.nih.gov) databases. CSMD2expression and its prognostic value were analyzed using bioinformatics methods. CSMD2 mRNA level in patients with BC and BC cell lines was evaluated via quantitative reverse transcriptase polymerase chain reaction. CSMD2 protein level in patients with BC was evaluated via immunohistochemistry. BC cell lines T24 and UMUC-3 were selected for loss-of-function assays targeting CSMD2. Cell viability was determined by CCK8 and clone formation experiments. Cell migration and invasion were evaluated using Transwell assays. Furthermore, the transcriptome of UMUC-3 with CSMD2 knockdown was sequenced to analyze potential signaling network pathways. Finally, the TIMER2.0 database was employed to identify the correlation between CSMD2 and immune cells in the tumor microenvironment.
UNASSIGNED: CSMD2 expression was up-regulated in BC tissues compared to adjacent tissues. High CSMD2 expression was associated with poor survival and could serve as an independent predictor for survival in patients with BC. Furthermore, down-regulation of CSMD2 notably restrained the viability, migration, and invasion abilities of T24 and UMUC-3 cells. Moreover, transcriptomic sequencing after CSMD2 knockdown in UMUC-3 cells revealed its involvement in the regulation of the malignant phenotype in BC. Finally, public databases suggest a connection between CSMD2 and immune cell infiltration in BC.
UNASSIGNED: These findings suggest that CSMD2 may promote proliferation and tumorigenicity, and could represent a potential target for improving the prognosis of BC.
UNASSIGNED: Public data were obtained from the TCGA (https://cancergenome.nih.gov) databases. CSMD2expression and its prognostic value were analyzed using bioinformatics methods. CSMD2 mRNA level in patients with BC and BC cell lines was evaluated via quantitative reverse transcriptase polymerase chain reaction. CSMD2 protein level in patients with BC was evaluated via immunohistochemistry. BC cell lines T24 and UMUC-3 were selected for loss-of-function assays targeting CSMD2. Cell viability was determined by CCK8 and clone formation experiments. Cell migration and invasion were evaluated using Transwell assays. Furthermore, the transcriptome of UMUC-3 with CSMD2 knockdown was sequenced to analyze potential signaling network pathways. Finally, the TIMER2.0 database was employed to identify the correlation between CSMD2 and immune cells in the tumor microenvironment.
UNASSIGNED: CSMD2 expression was up-regulated in BC tissues compared to adjacent tissues. High CSMD2 expression was associated with poor survival and could serve as an independent predictor for survival in patients with BC. Furthermore, down-regulation of CSMD2 notably restrained the viability, migration, and invasion abilities of T24 and UMUC-3 cells. Moreover, transcriptomic sequencing after CSMD2 knockdown in UMUC-3 cells revealed its involvement in the regulation of the malignant phenotype in BC. Finally, public databases suggest a connection between CSMD2 and immune cell infiltration in BC.
UNASSIGNED: These findings suggest that CSMD2 may promote proliferation and tumorigenicity, and could represent a potential target for improving the prognosis of BC.
摘要：
■CSMD2已被报道为几种癌症的潜在预后因素。然而,CSMD2是否影响膀胱癌(BC)尚不清楚.
■公开数据来自TCGA（https://cancergenome。nih.gov)数据库。使用生物信息学方法分析CSMD2的表达及其预后价值。通过定量逆转录酶聚合酶链反应评估BC和BC细胞系患者的CSMD2mRNA水平。通过免疫组织化学评估BC患者的CSMD2蛋白水平。选择BC细胞系T24和UMUC-3用于靶向CSMD2的功能丧失测定。通过CCK8和克隆形成实验确定细胞活力。使用Transwell测定法评估细胞迁移和侵袭。此外，对具有CSMD2敲低的UMUC-3转录组进行测序,以分析潜在的信号网络通路.最后,我们利用TIMER2.0数据库鉴定CSMD2与肿瘤微环境中免疫细胞之间的相关性.
■CSMD2表达在BC组织中与邻近组织相比上调。CSMD2高表达与低生存率相关，可作为BC患者生存率的独立预测因子。此外，CSMD2的下调显著抑制了生存能力，迁移,T24和UMUC-3细胞的侵袭能力。此外，在UMUC-3细胞中CSMD2敲低后的转录组测序显示其参与了BC中恶性表型的调节。最后,公共数据库提示CSMD2与BC中免疫细胞浸润之间存在联系.
■这些发现表明CSMD2可能促进增殖和致瘤性，并可能成为改善BC预后的潜在目标。
■公开数据来自TCGA（https://cancergenome。nih.gov)数据库。使用生物信息学方法分析CSMD2的表达及其预后价值。通过定量逆转录酶聚合酶链反应评估BC和BC细胞系患者的CSMD2mRNA水平。通过免疫组织化学评估BC患者的CSMD2蛋白水平。选择BC细胞系T24和UMUC-3用于靶向CSMD2的功能丧失测定。通过CCK8和克隆形成实验确定细胞活力。使用Transwell测定法评估细胞迁移和侵袭。此外，对具有CSMD2敲低的UMUC-3转录组进行测序,以分析潜在的信号网络通路.最后,我们利用TIMER2.0数据库鉴定CSMD2与肿瘤微环境中免疫细胞之间的相关性.
■CSMD2表达在BC组织中与邻近组织相比上调。CSMD2高表达与低生存率相关，可作为BC患者生存率的独立预测因子。此外，CSMD2的下调显著抑制了生存能力，迁移,T24和UMUC-3细胞的侵袭能力。此外，在UMUC-3细胞中CSMD2敲低后的转录组测序显示其参与了BC中恶性表型的调节。最后,公共数据库提示CSMD2与BC中免疫细胞浸润之间存在联系.
■这些发现表明CSMD2可能促进增殖和致瘤性，并可能成为改善BC预后的潜在目标。
