Jia Jiwei, Guo Pei, Zhang Li, Kong Wenqing, Wang Fangfang
Department of Radiation Oncology, Yantai Yuhuangding Hospital, 20 Yuhuangding East Road, Yantai, Shandong 264000, China.
Department of Pathology, Yantai Yuhuangding Hospital, 20 Yuhuangding East Road, Yantai, Shandong 264000, China.
Anal Cell Pathol (Amst). 2023 May 31;2023:6833987. doi: 10.1155/2023/6833987. eCollection 2023.
Colorectal cancer (CRC) substantially contributes to cancer-related deaths worldwide. Recently, a long non-coding RNA (lncRNA), LINC01614, has emerged as a vital gene regulator in cancer progression. Yet, how LINC01614 affects CRC progression remains enigmatic. Here, we defined LINC01614 expression in CRC, investigated the performance of CRC cells lacking LINC01614, and elucidated the underpinning mechanism. We observed that LINC01614 was upregulated in both CRC tissues and cell lines. LINC01614 knockdown repressed the proliferation and metastasis capacity of CRC cell lines. Consistently, an LINC01614 deficiency model exhibited slow tumor growth rate. Moreover, luciferase reporter assay, RNA pull-down, and immunoprecipitation confirmed that LINC01614 targeted miR-217-5p. LINC01614 knockdown reduced the expression of HMGA1 and N-cadherin, while increasing that of E-cadherin, resulting in decreased viability, proliferation, migration, and invasion capacity of CRC cells. Our results demonstrate that LINC01614 regulates CRC progression by modulating the miR-217-5p/HMGA1 axis, thus holding great potential as a prognostic biomarker for CRC diagnosis and treatment.
结直肠癌（CRC）在全球癌症相关死亡中占很大比例。最近，一种长链非编码RNA（lncRNA），即LINC01614，已成为癌症进展中的重要基因调节因子。然而，LINC01614如何影响CRC进展仍不清楚。在此，我们确定了CRC中LINC01614的表达，研究了缺乏LINC01614的CRC细胞的表现，并阐明了其潜在机制。我们观察到LINC01614在CRC组织和细胞系中均上调。敲低LINC01614可抑制CRC细胞系的增殖和转移能力。同样，LINC01614缺陷模型显示肿瘤生长速度缓慢。此外，荧光素酶报告基因检测、RNA下拉实验和免疫沉淀证实LINC01614靶向miR-217-5p。敲低LINC01614可降低HMGA1和N-钙黏蛋白的表达，同时增加E-钙黏蛋白的表达，导致CRC细胞的活力、增殖、迁移和侵袭能力下降。我们的结果表明，LINC01614通过调节miR-217-5p/HMGA1轴来调节CRC进展，因此作为CRC诊断和治疗的预后生物标志物具有巨大潜力。
