Zhu X, Luo X, Li T, Liang J, He J, Tang X
Department of General Surgery, Panyu District Central Hospital, Guangzhou 510000, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2022 Nov 20;42(11):1697-1704. doi: 10.12122/j.issn.1673-4254.2022.11.14.
To clarify the mechanism by which LINC01285 regulates proliferation and migration of colorectal cancer (CRC) cells and the clinical implications.
We analyzed the expression of LINC01285 in CRC tissues and normal tissues using data from Starbase public database. We also examined the expression levels of LINC01285 in 70 pairs of CRC and adjacent tissue samples collected from our center and in different CRC cell lines using RT-qPCR, and analyzed the correlation of LINC01285 expression with the clinicopathological parameters and tumor-free survival time of the patients. In CRC cell lines (SW620 and HT-29), the changes in cell proliferation, apoptosis, metastasis and epithelial-mesenchymal transition (EMT) phenotype following LINC01285 knockdown were analyzed using CCK-8 assay, flow cytometry, Transwell assay and Western blotting.
The TCGA-COAD transcriptome sequencing data obtained from the Starbasev3.0 public database revealed a significantly higher expression level of LINC01285 in CRC tissues than in adjacent tissues (=0.00016), which was verified by RT-qPCR results of the clinical samples (=0.0002). In CRC patients, the expression level of LINC01285 was closely correlated with histological differentiation of the tumor (=0.036), T classification (=0.000), lymph node metastasis (=0.001), TNM stage (=0.000), Duke stage (=0.009) and relapse-free survival (=0.0102). In SW620 and HT-29 cells, which expressed significantly higher levels of LINC01285 than normal colorectal mucosal cells ( < 0.001), LINC01285 knockdown significantly inhibited cell proliferation ( < 0.001), increased early apoptosis, late apoptosis and total apoptosis rates ( < 0.05), suppressed cell migration and invasion ( < 0.001), upregulated the expression of E-cadherin ( < 0.001), and downregulated the expression of N-cadherin ( < 0.001).
The expression level of LINC01285, which modulates the EMT pathway to regulate the proliferation, apoptosis and metastasis of CRC cells, is closely correlated with the prognosis of CRC patients.
阐明LINC01285调控结直肠癌（CRC）细胞增殖和迁移的机制及其临床意义。
利用Starbase公共数据库的数据，分析LINC01285在CRC组织和正常组织中的表达情况。我们还采用RT-qPCR检测了从本中心收集的70对CRC及其癌旁组织样本以及不同CRC细胞系中LINC01285的表达水平，并分析了LINC01285表达与患者临床病理参数及无瘤生存时间的相关性。在CRC细胞系（SW620和HT-29）中，利用CCK-8法、流式细胞术、Transwell法和蛋白质免疫印迹法分析敲低LINC01285后细胞增殖、凋亡、转移及上皮-间质转化（EMT）表型的变化。
从Starbasev3.0公共数据库获得的TCGA-COAD转录组测序数据显示，CRC组织中LINC01285的表达水平显著高于癌旁组织（=0.00016），临床样本的RT-qPCR结果验证了这一点（=0.0002）。在CRC患者中，LINC01285的表达水平与肿瘤的组织学分化（=0.036）、T分期（=0.000）、淋巴结转移（=0.001）、TNM分期（=0.000）、Duke分期（=0.009）及无复发生存（=0.0102）密切相关。在LINC01285表达水平显著高于正常结直肠黏膜细胞的SW620和HT-29细胞中（<0.001），敲低LINC01285可显著抑制细胞增殖（<0.001），增加早期凋亡、晚期凋亡及总凋亡率（<0.05），抑制细胞迁移和侵袭（<0.001），上调E-钙黏蛋白的表达（<0.001），下调N-钙黏蛋白的表达（<0.001）。
LINC01285的表达水平通过调节EMT途径调控CRC细胞的增殖、凋亡和转移，与CRC患者的预后密切相关。
