PDF(Pubmed)
Abstract：
UNASSIGNED: Research has demonstrated that apolipoprotein L1 (APOL1) has a role in the emergence and progression of a number of malignant cancers. It is unclear, however, how APOL1 functions in colorectal cancer (CRC). In this study, we examined the possible molecular processes underlying APOL1\'s biological role in CRC.
UNASSIGNED: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to identify APOL1 expression in patients with CRC and the cell line of cancer tissue. Following transfection of human colon carcinoma cells (HCT116) and human colon adenocarcinoma cells (SW1116) with sh-APOL1, the effects of APOL1 on the biological behavior of CRC cell lines were examined. In nude mice, the effect of APOL1 on tumor growth was noted. The protein interaction between APOL1 and RUNX1 was detected via coimmunoprecipitation. The expression of relevant proteins and cell biological behaviors were examined to confirm the APOL1-RUNX1 pathway in CRC cell lines.
UNASSIGNED: The CRC tissues and cells exhibited elevated expression of APOL1. HCT116 and SW1116 cells\' proliferation, migration, and invasion were suppressed by sh-APOL1, and sh-APOL1 also increased the expression of E-cadherin and decreased the expression of RUNX1, cyclin D1, β-catenin, N-cadherin, and vimentin. APOL1 bound to the RUNX1 protein and regulated its protein levels. The counteractive effect of sh-APOL1 epithelial-mesenchymal transition (EMT), proliferation, migration, and invasion of CRC cells was counteracted by the overexpression of RUNX1. By silencing APOL1, the Wnt-β-catenin pathway was able to restrain EMT and regulate the biological behavior processes in CRC cells.
UNASSIGNED: APOL1 has potential as a diagnostic biomarker for CRC. By preventing the Wnt-β-catenin pathway from being activated, the sh-APOL1-binding protein RUNX1 inhibited the EMT and biological behavior of CRC cells.
UNASSIGNED: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to identify APOL1 expression in patients with CRC and the cell line of cancer tissue. Following transfection of human colon carcinoma cells (HCT116) and human colon adenocarcinoma cells (SW1116) with sh-APOL1, the effects of APOL1 on the biological behavior of CRC cell lines were examined. In nude mice, the effect of APOL1 on tumor growth was noted. The protein interaction between APOL1 and RUNX1 was detected via coimmunoprecipitation. The expression of relevant proteins and cell biological behaviors were examined to confirm the APOL1-RUNX1 pathway in CRC cell lines.
UNASSIGNED: The CRC tissues and cells exhibited elevated expression of APOL1. HCT116 and SW1116 cells\' proliferation, migration, and invasion were suppressed by sh-APOL1, and sh-APOL1 also increased the expression of E-cadherin and decreased the expression of RUNX1, cyclin D1, β-catenin, N-cadherin, and vimentin. APOL1 bound to the RUNX1 protein and regulated its protein levels. The counteractive effect of sh-APOL1 epithelial-mesenchymal transition (EMT), proliferation, migration, and invasion of CRC cells was counteracted by the overexpression of RUNX1. By silencing APOL1, the Wnt-β-catenin pathway was able to restrain EMT and regulate the biological behavior processes in CRC cells.
UNASSIGNED: APOL1 has potential as a diagnostic biomarker for CRC. By preventing the Wnt-β-catenin pathway from being activated, the sh-APOL1-binding protein RUNX1 inhibited the EMT and biological behavior of CRC cells.
摘要：
■研究表明，载脂蛋白L1（APOL1）在许多恶性肿瘤的出现和发展中起作用。不清楚,然而,APOL1在结直肠癌（CRC）中的作用。在这项研究中,我们研究了APOL1在CRC中生物学作用的潜在分子过程。
■定量实时聚合酶链反应（qRT-PCR）用于鉴定CRC患者和癌组织细胞系中的APOL1表达。用sh-APOL1转染人结肠癌细胞（HCT116）和人结肠腺癌细胞（SW1116）后，检查了APOL1对CRC细胞系生物学行为的影响。在裸鼠中，观察到APOL1对肿瘤生长的影响.通过共免疫沉淀检测APOL1和RUNX1之间的蛋白质相互作用。检测了相关蛋白的表达和细胞生物学行为，以确认CRC细胞系中APOL1-RUNX1途径。
■CRC组织和细胞显示APOL1的表达升高。HCT116和SW1116细胞增殖，迁移,和侵袭被sh-APOL1抑制，sh-APOL1还增加了E-cadherin的表达，并降低了RUNX1，cyclinD1，β-catenin的表达，N-钙黏着蛋白,还有波形蛋白.APOL1与RUNX1蛋白结合并调节其蛋白水平。SH-APOL1上皮间质转化（EMT）的反作用，扩散,迁移,并且CRC细胞的侵袭被RUNX1的过表达所抵消。通过沉默APOL1，Wnt-β-catenin通路能够抑制EMT并调节CRC细胞的生物学行为过程。
■APOL1具有作为CRC诊断生物标志物的潜力。通过阻止Wnt-β-catenin通路被激活,sh-APOL1结合蛋白RUNX1抑制CRC细胞的EMT和生物学行为。
■定量实时聚合酶链反应（qRT-PCR）用于鉴定CRC患者和癌组织细胞系中的APOL1表达。用sh-APOL1转染人结肠癌细胞（HCT116）和人结肠腺癌细胞（SW1116）后，检查了APOL1对CRC细胞系生物学行为的影响。在裸鼠中，观察到APOL1对肿瘤生长的影响.通过共免疫沉淀检测APOL1和RUNX1之间的蛋白质相互作用。检测了相关蛋白的表达和细胞生物学行为，以确认CRC细胞系中APOL1-RUNX1途径。
■CRC组织和细胞显示APOL1的表达升高。HCT116和SW1116细胞增殖，迁移,和侵袭被sh-APOL1抑制，sh-APOL1还增加了E-cadherin的表达，并降低了RUNX1，cyclinD1，β-catenin的表达，N-钙黏着蛋白,还有波形蛋白.APOL1与RUNX1蛋白结合并调节其蛋白水平。SH-APOL1上皮间质转化（EMT）的反作用，扩散,迁移,并且CRC细胞的侵袭被RUNX1的过表达所抵消。通过沉默APOL1，Wnt-β-catenin通路能够抑制EMT并调节CRC细胞的生物学行为过程。
■APOL1具有作为CRC诊断生物标志物的潜力。通过阻止Wnt-β-catenin通路被激活,sh-APOL1结合蛋白RUNX1抑制CRC细胞的EMT和生物学行为。
