Department of Colorectal Surgery, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, Zhejiang, China.
Eur Rev Med Pharmacol Sci. 2020 Aug;24(16):8439-8446. doi: 10.26355/eurrev_202008_22641.
To detect the expression level of long intergenic non-protein coding RNA 1198 (LINC01198) in colorectal cancer (CRC) tissues and cells, to investigate the effect of LINC01198 on the biological function of CRC cells through in vivo and in vitro experiments, and to explore its molecular mechanism.
Tissue samples were collected from 32 patients with CRC. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to detect the relative expression level of LINC01198 in CRC tissues and cells. In vitro experiments [Cell Counting Kit-8 (CCK-8) and flow cytometry] were conducted to explore the effect of interfering with the expression of LINC01198 on the proliferation, cycle and apoptosis of CRC cells. Tumorigenesis assay was undertaken in nude mice to investigate the influence of LINC01198 on the tumorigenic ability of CRC cells in vivo. Besides, Western blotting was performed to determine the changes in the downstream signaling pathway of LINC01198.
Among the 32 cases of tissue samples of CRC patients, 28 cases had an upregulated expression of LINC01198 compared with paracancerous tissues. The results of qRT-PCR indicated that LINC01198 expression was upregulated in CRC cells, and the interference efficiency of si-LINC01198 was measured via qRT-PCR. The results of in vitro experiments demonstrated that after interfering with the expression of LINC01198 in CRC cells, cell proliferation capacity was inhibited, cell cycle was arrested at G1/G0 phase, and the apoptosis rate was increased. The results of nude mice tumorigenesis experiments revealed that after interfering with the expression of LINC01198, the tumorigenic ability of CRC cells in vivo declined. Additionally, Western blotting assay results confirmed that after interfering with the expression of LINC01198, the expression of molecular markers in the Notch signaling pathway was inhibited.
The expression of LINC01198 is upregulated in the case of CRC, which promotes proliferation and inhibits apoptosis of CRC cells by regulating the Notch signaling pathway. Our findings provide a novel biomarker for the diagnosis and treatment of HCC patients and treatment strategies.
检测长链非编码 RNA 1198（LINC01198）在结直肠癌（CRC）组织和细胞中的表达水平，通过体内和体外实验研究 LINC01198 对 CRC 细胞生物学功能的影响，并探讨其分子机制。
收集 32 例 CRC 患者的组织样本。采用实时荧光定量聚合酶链反应（qRT-PCR）检测 CRC 组织和细胞中 LINC01198 的相对表达水平。体外实验[细胞计数试剂盒-8（CCK-8）和流式细胞术]探讨干扰 LINC01198 表达对 CRC 细胞增殖、周期和凋亡的影响。裸鼠成瘤实验研究 LINC01198 对 CRC 细胞体内致瘤能力的影响。此外，Western blot 检测 LINC01198 下游信号通路的变化。
在 32 例 CRC 患者的组织样本中，28 例与癌旁组织相比，LINC01198 表达上调。qRT-PCR 结果表明 LINC01198 在 CRC 细胞中表达上调，并通过 qRT-PCR 测量了 si-LINC01198 的干扰效率。体外实验结果表明，干扰 CRC 细胞中 LINC01198 的表达后，细胞增殖能力受到抑制，细胞周期停滞在 G1/G0 期，凋亡率增加。裸鼠成瘤实验结果表明，干扰 LINC01198 表达后，CRC 细胞体内的致瘤能力下降。此外，Western blot 检测结果证实，干扰 LINC01198 表达后，Notch 信号通路中的分子标记物表达受到抑制。
CRC 中 LINC01198 的表达上调，通过调节 Notch 信号通路促进 CRC 细胞的增殖和抑制凋亡。我们的研究结果为 HCC 患者的诊断和治疗提供了新的标志物和治疗策略。
