ArticleJournal of clinical laboratory analysis2021
The long non-coding RNA PCAL7 promotes prostate cancer by strengthening androgen receptor signaling.
Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Long Non-Coding RNAs, Nuclear Receptors and Their Cross-Talks in Cancer-Implications and Perspectives.Cancers · 2024Review
- Endocrine nuclear receptors and long non‑coding RNAs reciprocal regulation in cancer (Review).International journal of oncology · 2024Review
- Interaction between Non-Coding RNAs and Androgen Receptor with an Especial Focus on Prostate Cancer.Cells · 2021Review
- Emerging role of long noncoding RNAs in recurrent hepatocellular carcinoma.World journal of clinical cases · 2021Review
- LncRNA FGF14-AS2 represses growth of prostate carcinoma cells via modulating miR-96-5p/AJAP1 axis.Journal of clinical laboratory analysis · 2021Article
- The long non-coding RNA PCAL7 promotes prostate cancer by strengthening androgen receptor signaling.Journal of clinical laboratory analysis · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe prostate cancer (PCa) has been a global problem to men health. Notably, the androgen receptor (AR) is essential for both normal development of prostate and prostate cancer progression.
methodsThe RNA sequencing was used to identify the novel long non-coding RNA (lncRNA) termed PCAL7. The RT-qPCR was performed to quantify PCAL7 expression. Migration and proliferation assays were used to examine the function of PCAL7. Fluorescence in situ hybridization (FISH) was used to determine subcellular localization.
resultsBy RNA sequencing, the differentially expressed lncRNAs were identified (top 10 upregulated lncRNAs: PCAL7, AC083843.1, CTC-338M12.3, RP11-443B7.1, RP11-1008C21.2, RN7SL329P, RP4-773N10.4, RP11-264B17.2, KB-1507C5.2, and RP11-20B24.6; top 10 downregulated lncRNAs: RP11-77H9.2, RAB11FIP1P1, AP001625.6, CTA-217C2.1, RP11-603J24.7, RP11-315I20.1, AC092839.1, RP4-758J18.10, RP11-259O2.3, and HMGN2P17). PCAL7 was the lncRNA with the highest fold upregulation and significantly correlated with AR signaling during prostate cancer progression. The AR-regulated PCAL7 was abundantly overexpressed in prostate cancer tissues and AR-dependent cell lines. PCAL7 knockdown inhibited cell migration and proliferation. Consistently, the migration and proliferation were promoted by PCAL7 overexpression. PCAL7 depletion via antisense oligonucleotides (ASOs) markedly suppressed AR signaling and tumor growth. Mechanistically, PCAL7 interacted with Huntingtin-interacting protein 1 (HIP1) to stabilize HIP1. Therefore, PCAL7 could advance AR signaling via a novel positive feedback loop.
conclusionOur experiments support an oncogenic role for PCAL7 which promotes prostate cancer progression suggesting PCAL7 may serve as a potential therapeutic target.
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