Department of Colorectal Surgery, Heping Hospital Affiliated to Changzhi Medical College, Changzhi City, Shanxi Province 046000, PR China.
Department of Colorectal Surgery, Heping Hospital Affiliated to Changzhi Medical College, Changzhi City, Shanxi Province 046000, PR China.
Arab J Gastroenterol. 2022 May;23(2):65-69. doi: 10.1016/j.ajg.2021.11.001. Epub 2022 Apr 26.
It has been reported that long non-coding RNA (lncRNA) AK077216 involves in osteoclastogenesis and bone resorption. Our preliminary data has revealed that AK077216 was downregulated in colorectal adenocarcinoma (CRA) and it was closely correlated with miR-34a. This study was carried out to explore the role of AK077216 in CRA with a focus on its interactions with miR-34a.
Paired CRA and non-tumor tissues collected from 66 CRA patients were subjected to RNA preparations, followed by RT-qPCRs to determine the expression levels of AK077216 and miR-34a. The interactions between AK077216 and miR-34a were analyzed with overexpression assays. Transwell assays were carried out to explore the roles of AK077216 and miR-34a in regulating CRA cell invasion and migration.
AK077216 was downregulated in CRA tissues compared to that in non-tumor tissues of CRA patients. During a 5-year follow-up, patients with lower expression levels of AK077216 in CRA tissues showed significantly lower overall survival. MiR-34a was upregulated in CRA tissues and inversely correlated with AK077216. Overexpression of AK077216 decreased the expression levels of miR-34a, while overexpression of miR-34a did not affect the expression of AK077216. Overexpression of AK077216 inhibited CRA cell migration and invasion, while overexpression of miR-34a accelerated cancer cell migration and invasion and attenuated the effects of overexpression on AK077216 on cell behaviors.
Therefore, AK077216 may inhibit CRA cell migration and invasion by downregulating miR-34a.
据报道，长链非编码 RNA（lncRNA）AK077216 参与破骨细胞生成和骨吸收。我们的初步数据显示，AK077216 在结直肠腺癌（CRA）中下调，且与 miR-34a 密切相关。本研究旨在探讨 AK077216 在 CRA 中的作用，重点研究其与 miR-34a 的相互作用。
收集 66 例 CRA 患者的配对 CRA 和非肿瘤组织，进行 RNA 提取，随后进行 RT-qPCR 检测 AK077216 和 miR-34a 的表达水平。通过过表达实验分析 AK077216 和 miR-34a 之间的相互作用。采用 Transwell 实验探讨 AK077216 和 miR-34a 在调节 CRA 细胞侵袭和迁移中的作用。
与 CRA 患者的非肿瘤组织相比，AK077216 在 CRA 组织中下调。在 5 年的随访中，AK077216 在 CRA 组织中表达水平较低的患者总生存率显著降低。miR-34a 在 CRA 组织中上调，与 AK077216 呈负相关。AK077216 的过表达降低了 miR-34a 的表达水平，而过表达 miR-34a 不影响 AK077216 的表达。AK077216 的过表达抑制了 CRA 细胞的迁移和侵袭，而过表达 miR-34a 加速了癌细胞的迁移和侵袭，并减弱了 AK077216 过表达对细胞行为的影响。
因此，AK077216 可能通过下调 miR-34a 抑制 CRA 细胞的迁移和侵袭。
