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Objective <p>To investigate the clinical value and mechanism of action of long non-coding RNA PRKCQ-AS1 for lung adenocarcinoma (LUAD) progression.</p> Methods <p>Clinical data of 128 LUAD patients were collected, postoperative pathological tissues were stored at -80&#xa0;°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.</p> Results <p>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.</p> Conclusion <p>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.</p> Clinical trial number <p>Not applicable.</p>

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Clinical significance and biological function of PRKCQ-AS1/miR-582-3p expression in LUAD

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月1日

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  • Lingling Liu,
  • Xiaofen Liu,
  • Xiaojiao Wu,
  • Hang Fang,
  • Jingjing Shi,
  • Wei Jiang

摘要

Objective

To investigate the clinical value and mechanism of action of long non-coding RNA PRKCQ-AS1 for lung adenocarcinoma (LUAD) progression.

Methods

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.

Results

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.

Conclusion

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.

Clinical trial number

Not applicable.