长链非编码RNA LINC02178对膀胱癌细胞增殖、侵袭及迁移的影响及机制研究

Effects and mechanism of long non-coding RNA LINC02178 on proliferation, invasion and migration of bladder cancer cells

  • 摘要:
    目的  探讨长链非编码RNA LINC02178对膀胱癌细胞增殖、侵袭、迁移的影响及机制。
    方法  基于公共数据库分析LINC02178在膀胱癌组织中的表达水平。采用逆转录-实时定量聚合酶链反应(RT-qPCR)检测LINC02178在膀胱癌细胞中的表达; 采用si-LINC02178、si-NC片段转染J82细胞; 采用噻唑蓝(MTT)实验和Transwell法检测沉默LINC02178后细胞增殖、侵袭和迁移能力的变化; 采用Western blot检测磷脂酰肌醇-3-激酶(PI3K)、磷酸化PI3K(p-PI3K)、蛋白激酶B(Akt)、磷酸化Akt(p-Akt)蛋白的表达水平。
    结果  LINC02178在膀胱癌组织中高表达,且高表达患者生存预后较低表达患者更差,差异有统计学意义(P < 0.05)。LINC02178在膀胱癌细胞J82、T24、5637中的表达水平高于膀胱正常上皮细胞,差异有统计学意义(P < 0.05)。si-LINC02178组细胞增殖能力弱于si-NC组,差异有统计学意义(P < 0.05)。si-LINC02178和si-NC组细胞侵袭数分别为(91.33±2.02)、(179.30±4.26)个,迁移数分别为(98.33±3.84)、(196.30±2.73)个,差异均有统计学意义(P < 0.05)。沉默LINC02178后,细胞中p-PI3K、p-Akt蛋白的表达下调,差异有统计学意义(P < 0.05),而PI3K、Akt蛋白无显著变化(P>0.05)。
    结论  LINC02178表达与膀胱癌患者预后不良有关,沉默LINC02178可抑制膀胱癌细胞增殖、侵袭和迁移,其机制可能是通过PI3K/Akt信号通路进行调控。

     

    Abstract:
    Objective  To investigate the expression of long non-coding RNA LINC02178 in bladder cancer and its effects on the proliferation, invasion and migration of bladder cancer cells.
    Methods  The expression level of LINC02178 in bladder cancer tissues was analyzed based on the public database. The expression of LINC02178 in bladder cancer cells was detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Si-LINC02178 and si-NC fragments were transfected into J82 cells, and the changes of proliferation, invasion and migration of the expression of LINC02178 after silencing were detected by Methyl Thiazolyl Tetrazolium (MTT) and Transwell methods. The protein expression levels of phosphatidylinositol-3-kinase (PI3K), phosphorylated PI3K(p-PI3K), protein kinase B(Akt), phosphorylated Akt(p-Akt) protein were detected by Western blot.
    Results  LINC02178 was highly expressed in bladder cancer tissues, and the survival prognosis of patients with high expression was worse compared with those with low expression (P < 0.05). The expression of LINC02178 in bladder cancer cell lines J82, T24 and 5637 was significantly higher than that in normal bladder epithelial cells (P < 0.05). The cell proliferation ability of the si-LINC02178 group was lower than that of the si-NC group (P < 0.05). The number of cells invaded in the si-LINC02178 group and si-NC group was (91.33±2.02) and (179.30±4.26), and the number of cells migrated was (98.33±3.84) and (196.30±2.73), respectively, which showed statistically significant difference between the two groups (P < 0.05). After silencing LINC02178, the expression of p-PI3K and p-Akt protein in cells was down-regulated, while PI3K and Akt had no significant changes (P>0.05).
    Conclusion  LINC02178 expression is associated with poor prognosis of patients with bladder cancer. Silencing LINC02178 expression can inhibit the proliferation, invasion and migration of bladder cancer cells, which may be regulated by the PI3K/Akt signaling pathway.

     

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