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

  • 0Integrated Chinese and Western Medicine Oncology, the First Hospital of Qiqihar, Qiqihar, 161000, China.
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July 2, 2025

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July 2, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Long non-coding RNA PRKCQ-AS1 is down-regulated in lung adenocarcinoma (LUAD), and its low expression correlates with poor survival. PRKCQ-AS1 targets miR-582-3p, inhibiting LUAD cell proliferation, migration, and invasion.

Area Of Science

  • Oncology
  • Molecular Biology
  • Genetics

Background

  • Lung adenocarcinoma (LUAD) is a major cause of cancer-related mortality.
  • Long non-coding RNAs (lncRNAs) play crucial roles in cancer progression, but their specific functions in LUAD remain incompletely understood.
  • Identifying novel molecular targets is essential for improving LUAD diagnosis and treatment.

Purpose Of The Study

  • To investigate the clinical significance and underlying mechanism of long non-coding RNA PRKCQ-AS1 in the progression of lung adenocarcinoma (LUAD).
  • To elucidate the regulatory relationship between PRKCQ-AS1 and microRNA-582-3p (miR-582-3p) in LUAD.
  • To assess the impact of PRKCQ-AS1 on LUAD cell proliferation, migration, and invasion.

Main Methods

  • Collected clinical data and pathological tissues from 128 LUAD patients.
  • Utilized Kaplan-Meier survival analysis and Cox regression models to evaluate prognostic factors.
  • Employed reverse transcription quantitative PCR (RT-qPCR) to measure PRKCQ-AS1 and miR-582-3p expression.
  • Performed dual-luciferase reporter assays, CCK8, and Transwell assays to validate molecular interactions and assess cellular functions.

Main Results

  • PRKCQ-AS1 was found to be significantly down-regulated, while miR-582-3p was up-regulated in LUAD tissues and cells.
  • Low PRKCQ-AS1 expression and high miR-582-3p expression were associated with adverse pathological features and increased patient mortality.
  • PRKCQ-AS1 directly targets miR-582-3p, and this interaction influences LUAD cell proliferation, migration, and invasion. Downstream targets RGMB and STXBP6 were identified.
  • Overexpression of PRKCQ-AS1 inhibited LUAD cell growth and metastasis, effects that were reversed by miR-582-3p mimics.

Conclusions

  • A regulatory axis between PRKCQ-AS1 and miR-582-3p is established in lung adenocarcinoma.
  • PRKCQ-AS1 functions as a tumor suppressor by targeting miR-582-3p, thereby regulating the proliferation, migration, and invasion of LUAD cells.
  • PRKCQ-AS1 holds potential as a therapeutic target for lung adenocarcinoma.

Keywords:

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