Liu Lingling, Liu Xiaofen, Wu Xiaojiao, Fang Hang, Shi Jingjing, Jiang Wei
Integrated Chinese and Western Medicine Oncology, the First Hospital of Qiqihar, Qiqihar, 161000, China.
Department of Respiratory and Critical Care Medicine, Taikang Tongji (Wuhan) Hospital, Wuhan, 430050, China.
Hereditas. 2025 Jul 1;162(1):116. doi: 10.1186/s41065-025-00482-9.
To investigate the clinical value and mechanism of action of long non-coding RNA PRKCQ-AS1 for lung adenocarcinoma (LUAD) progression.
Clinical data of 128 LUAD patients were collected, postoperative pathological tissues were stored at -80 °C. Kaplan-Meier survival analysis was employed to investigate differences in 5-year survival rates across various expression groups, while Cox regression models assessed the prognostic factors influencing patient outcomes. Reverse transcription quantitative PCR (RT-qPCR) was utilized to measure the expression levels of PRKCQ-AS1 and miR-582-3p in pathological tissues and LUAD cell lines. Additionally, a dual-luciferase reporter assay validated the reciprocal relationship. CCK8 examined cell proliferation, Transwell observed cell migration and invasion.
PRKCQ-AS1 was down-regulated and miR-582-3p was up-regulated in LUAD tissues and cell. PRKCQ-AS1 and miR-582-3p expression affects some pathological features (lymph node metastasis, TNM stage, tumour differentiation) in LUAD patients. Patients with low PRKCQ-AS1 and high miR-582-3p had increased mortality. Interaction of PRKCQ-AS1 targeting miR-582-3p exists in LUAD cells. RGMB, STXBP6 are downstream target genes of miR-582-3p. Overexpression of (oe-) PRKCQ-AS1 inhibited LUAD cell proliferation, migration, and invasion. However, concomitant use of miR-582-3p mimics resisted the effects of PRKCQ-AS1 overexpression on cells.
PRKCQ-AS1/miR-582-3p axis regulatory relationship exists in lung adenocarcinoma cells. PRKCQ-AS1 may regulate the proliferation, migration and invasion of lung adenocarcinoma cells and participate in LUAD regulation by targeting miR-582-3p.
Not applicable.
探讨长链非编码RNA PRKCQ-AS1在肺腺癌（LUAD）进展中的临床价值及作用机制。
收集128例LUAD患者的临床资料，术后病理组织保存于-80°C。采用Kaplan-Meier生存分析研究不同表达组5年生存率的差异，同时用Cox回归模型评估影响患者预后的因素。利用逆转录定量PCR（RT-qPCR）检测病理组织和LUAD细胞系中PRKCQ-AS1和miR-582-3p的表达水平。此外，双荧光素酶报告基因检测验证了二者的相互关系。CCK8检测细胞增殖，Transwell观察细胞迁移和侵袭。
PRKCQ-AS1在LUAD组织和细胞中表达下调，miR-582-3p表达上调。PRKCQ-AS1和miR-582-3p的表达影响LUAD患者的一些病理特征（淋巴结转移、TNM分期、肿瘤分化）。PRKCQ-AS1低表达和miR-582-3p高表达的患者死亡率增加。在LUAD细胞中存在PRKCQ-AS1靶向miR-582-3p的相互作用。RGMB、STXBP6是miR-582-3p的下游靶基因。过表达（oe-）PRKCQ-AS1可抑制LUAD细胞的增殖、迁移和侵袭。然而，同时使用miR-582-3p模拟物可抵抗PRKCQ-AS1过表达对细胞的影响。
肺腺癌细胞中存在PRKCQ-AS1/miR-582-3p轴调控关系。PRKCQ-AS1可能通过靶向miR-582-3p调控肺腺癌细胞的增殖、迁移和侵袭，并参与LUAD的调控。
不适用。
