Open AccessThe long non‐coding RNA PCAL7 promotes prostate cancer by strengthening androgen receptor signaling
Author(s) -
Li Zhihui,
Teng Jingfei,
Jia Zhuomin,
Zhang Guohui,
Ai Xing
Publication year - 2021
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23645
Subject(s) - prostate cancer , gene knockdown , androgen receptor , cancer research , downregulation and upregulation , long non coding rna , biology , cell growth , tumor progression , rna , signal transduction , prostate , cancer , microbiology and biotechnology , apoptosis , gene , genetics
Background The 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. Methods The 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. Results By 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. Conclusion Our experiments support an oncogenic role for PCAL7 which promotes prostate cancer progression suggesting PCAL7 may serve as a potential therapeutic target.