ArticleHereditas2025
Clinical significance and biological function of PRKCQ-AS1/miR-582-3p expression in LUAD.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Reannotation of Public Transcriptomic Data Identifies Candidate lncRNAs and Putative Regulatory Networks in Rhabdomyosarcoma.Biomedicines · 2026Article
- Analysis of the mechanism and prognostic value of PRKCQ-AS1 in inhibiting the progression of lung adenocarcinoma via regulating the PD-1/PD-L1 pathway.Scientific reports · 2026Article
- LINC01980 promotes the malignant progression of lung squamous carcinoma by targeting miR-204-3p.Hereditas · 2025Article
- Mechanistic studies ofFrontiers in oncology · 2025Article
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6 authors.
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Abstract
objectiveTo investigate the clinical value and mechanism of action of long non-coding RNA PRKCQ-AS1 for lung adenocarcinoma (LUAD) progression.
methodsClinical 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.
resultsPRKCQ-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.
conclusionPRKCQ-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.
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