Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei, China.
Department of Gastrointestinal Surgery, Xi'an No. 3 Hospital, the Affiliated Hospital of Northwest University, Xi'an, Shaanxi Province, China.
Bioengineered. 2022 Mar;13(3):5357-5372. doi: 10.1080/21655979.2021.2018972.
MicroRNA-363-3p (miR-363-3p), reportedly, exhibits a tumor-suppressive role in human malignancies. Herein, our research was designed to further explain the functions and molecular mechanisms of miR-363-3p in the progression of colorectal cancer (CRC). With in vitro models, this study found that miR-363-3p was markedly under-expressed in CRC tissues and cells, and its overexpression suppressed the viability, migration, and invasion of CRC cells, and promoted cell apoptosis, whereas inhibiting miR-363-3p expression exhibited an opposite role. Additionally, aurora kinase A (AURKA), capable of counteracting the impacts of miR-363-3p on malignant biological behaviors of CRC cells, was identified as a direct target of miR-363-3p. Besides, miR-363-3p was sponged by long non-coding RNA small nucleolar RNA host gene 5 (SNHG5), which suppressed miR-363-3p expression. This research shows that SNHG5/miR-363-3p/AURKA axis partakes in CRC progression.
microRNA-363-3p(miR-363-3p)据报道,在人类恶性肿瘤中具有肿瘤抑制作用。在此,我们的研究旨在进一步解释 miR-363-3p 在结直肠癌(CRC)进展中的功能和分子机制。通过体外模型,本研究发现 miR-363-3p 在 CRC 组织和细胞中明显低表达,其过表达抑制 CRC 细胞的活力、迁移和侵袭,并促进细胞凋亡,而抑制 miR-363-3p 表达则起到相反的作用。此外,鉴定出极光激酶 A(AURKA)是 miR-363-3p 对 CRC 细胞恶性生物学行为的影响的直接靶点,能够抵消 miR-363-3p 的作用。此外,长链非编码 RNA 小核仁 RNA 宿主基因 5(SNHG5)可以吸附 miR-363-3p,从而抑制 miR-363-3p 的表达。本研究表明,SNHG5/miR-363-3p/AURKA 轴参与 CRC 的进展。