FOXD2-AS1 inhibits the proliferation and migration in prostate cancer: an in vitro and in vivo study
FOXD2 Adjacent Opposite Strand RNA 1 (FOXD2-AS1), a long noncoding RNA (lncRNA), exhibits specifically elevated in numerous cancerous cells. Numerous studies have shown that FOXD2-AS1 encourages cellular proliferation, migration and invasion. Nevertheless, the exact mechanism through which FOXD2-...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MRE Press
2023-09-01
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| Series: | Journal of Men's Health |
| Subjects: | |
| Online Access: | https://oss.jomh.org/files/article/20230928-106/pdf/JOMH2023070601.pdf |
| Summary: | FOXD2 Adjacent Opposite Strand RNA 1 (FOXD2-AS1), a long
noncoding RNA (lncRNA), exhibits specifically elevated in numerous cancerous
cells. Numerous studies have shown that FOXD2-AS1 encourages cellular proliferation, migration and invasion.
Nevertheless, the exact mechanism through which FOXD2-AS1 contributes to
prostate cancer (PCa) remains unclear. Consequently, we aimed to explore the
implications of FOXD2-AS1 on the growth of PCa.
Initially, an elevation of FOXD2-AS1 observed in PCa cells (PC-3,
DU145 and Lncap) than the prostate normal cell line RWPE2. Then, PC-3 cells were tranafected with shFOXD2-AS1,
sh-Numerical Control (shNC) or FOXD2-AS1 to assess the implications of FOXD2-AS. Cell growth
was measured with cell counting kit-8 (CCK8) and 5-ethynyl-2′-deoxyuridine (EDU)
assays, and cell invasion and migration were assessed by Transwell assays, which
demonstrated that FOXD2-AS1 silence impeded proliferation, migration and
invasion of PC-3 cells. Additionally, we discovered that FOXD2-AS1
bonded with miR-206/programmed cell death protein 10 (PDCD10) trough analyzing the interaction sites of lncRNA,
miRNA and protein. Then, these interaction abilities were confirmed by
dual-luciferase reporter assays and RT-qPCR, suggesting FOXD2-AS1 could
upregulate the amount of PDCD10 through suppressing miR-206. Furthermore, the
role of FOXD2-AS1 silencing on PCa carcinogenesis were assessed.
In vivo experiment, shFOXD2-AS1 led to a notable reduction in both the size and weight of
PCa. These findings indicated that FOXD2-AS1 silencing effectively
hindered the progression of prostate cancer.
In conclusion, the upregulation of FOXD2-AS1 was
observed in PCa, and the knockdown of FOXD2-AS1 could alleviated tumor
development by targeting miR-206 to upregulate PDCD10 expression. |
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| ISSN: | 1875-6867 1875-6859 |