FOXD1‐AS1 promotes malignant behaviours of prostate cancer cells via the miR‐3167/YWHAZ axis

Herein, the effect of long noncoding RNA forkhead box D1 antisense RNA 1 (FOXD1‐AS1) on malignant phenotypes of prostate cancer (PCa) cells was investigated. FOXD1‐AS1 presented high expression in PCa cells according to the results of RT‐qPCR. As shown by cell counting kit‐8 assays, colony formation...

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Veröffentlicht in:Andrologia 2022-02, Vol.54 (1), p.e14263-n/a
Hauptverfasser: Qu, Weilong, Wei, Xuedong, Zhang, Haoyu, Hou, Jianquan
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Sprache:eng
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Zusammenfassung:Herein, the effect of long noncoding RNA forkhead box D1 antisense RNA 1 (FOXD1‐AS1) on malignant phenotypes of prostate cancer (PCa) cells was investigated. FOXD1‐AS1 presented high expression in PCa cells according to the results of RT‐qPCR. As shown by cell counting kit‐8 assays, colony formation assays, wound‐healing assays, Transwell assays and flow cytometry analyses, silenced FOXD1‐AS1 suppressed PCa cell viability, proliferation, migration and invasion and enhanced cell apoptosis. Additionally, FOXD1‐AS1 was primarily localised in cytoplasm of PCa cells. RNA immunoprecipitation assays and luciferase reporter assays revealed that FOXD1‐AS1 interacted with miR‐3167 in PCa cells. MiR‐3167 functioned as an anti‐oncogene in PCa and miR‐3167 overexpression suppressed cell proliferation while promoted cell apoptosis. Moreover, the downstream target of miR‐3167 is mRNA YWHAZ. FOXD1‐AS1 elevated the expression of YWHAZ by binding with miR‐3167. The suppressive effect of miR‐3167 on YWHAZ expression was reversed by FOXD1‐AS1 overexpression. Furthermore, overexpressed YWHAZ reversed the suppressive effect of FOXD1‐AS1 deficiency on malignant behaviours of PCa cells. Overall, FOXD1‐AS1 facilitates malignant phenotypes of PCa cells by up‐regulating YWHAZ via miR‐3167. The study first reveals the molecular mechanism of FOXD1‐AS1 in PCa, suggesting that FOXD1‐AS1 and its downstream molecules might be prognostic biomarkers before medical treatment.
ISSN:0303-4569
1439-0272
DOI:10.1111/and.14263