&lt;p&gt;miR-129-5p inhibits prostate cancer proliferation via targeting ETV1&lt;/p&gt;

Gao, Ge; Xiu, Dianhui; Yang, Bin; Sun, Daju; Wei, Xin; Ding, Yudi; Ma, Yanan; Wang, Zhixin

doi:10.2147/ott.s183435

Cited by 28 publications

(35 citation statements)

References 44 publications

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“…Meanwhile, the expression of miR‐129‐5p in the growth plate was also verified by in situ hybridization. Several studies 26,27 have indicated that miR‐129‐5p can inhibit the proliferation of prostate cancer cells, is expressed by osteoblasts in rheumatoid arthritis, 28 and can directly inhibit IL‐17 expression. Nevertheless, the expression of miR‐129‐5p in chondrocytes and growth plates has not yet been reported elsewhere.…”

Section: Discussionmentioning

confidence: 99%

Chondrocyte suppression is mediated by miR‐129‐5p via GDF11/SMAD3 signaling in developmental dysplasia of the hip

Liu

Deng

Ding

et al. 2020

Journal Orthopaedic Research

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Recent studies have shown that developmental dysplasia of the hip (DDH) during childhood and in animal models is associated with impaired endochondral ossification of the roof of the acetabulum, yet the molecular mechanism of this pathology remains unknown. To address this, an animal model of DDH was established in 4‐week‐old New Zealand white rabbits by cast immobilization of knee extension. Fifty‐six rabbits of DDH were involved in this study, including 21 male rabbits and 25 female rabbits. High‐throughput RNA sequencing identified 18 differentially expressed microRNAs; miR‐129‐5p downregulation was further confirmed by quantitative polymerase chain reaction. Bioinformatics and luciferase reporter assay identified growth differentiation factor 11 (GDF11) as the target gene of miR‐129‐5p in vitro. miR‐129‐5p downregulation increased GDF11 expression, which induced the phosphorylation of SMAD family member 3. As a result, the expression of runt‐related transcription factor 2, Indian hedgehog homolog, and collagen type X was inhibited in vitro. Meanwhile, Alizarin Red S and Von Kossa staining revealed reduced formation of mineralized nodules by chondrocytes after miR‐129‐5P downregulation compared with the control. Additionally, proliferation assays and flow cytometry confirmed the suppression of chondrocyte proliferation and G1 cell cycle arrest following miR‐129‐5p downregulation. These findings indicate that miR‐129‐5p is able to suppress chondrocyte proliferation and hypertrophic differentiation and decrease mineralization via the miR‐129‐5p/GDF11/SMAD3 axis. This could present the underlying cause for the observed DDH‐associated ossification impairment of the acetabular roof.

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Section: Discussionmentioning

confidence: 99%

Chondrocyte suppression is mediated by miR‐129‐5p via GDF11/SMAD3 signaling in developmental dysplasia of the hip

Liu

Deng

Ding

et al. 2020

Journal Orthopaedic Research

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“…Dual functions for miR-129, as a tumor suppressor and oncogene, have been confirmed in various types of carcinomas. miR-129-5p has been reported to be downregulated in neuroendocrine tumors, prostate cancer, lung cancer and gastric cancer and functions as a tumorsuppressor role in these carcinomas [22][23][24]. Epigenetic regulation of miR-129-2 was demonstrated in glioma and lung cancer [25,26].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-129-2-3p directly targets Wip1 to suppress the proliferation and invasion of intrahepatic cholangiocarcinoma

Chen¹,

Jiang²,

Fang³

et al. 2020

J. Cancer

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Accumulated studies showed that numerous microRNAs (miRNAs) were aberrantly expressed in human intrahepatic cholangiocarcinoma (ICC) and contributed to the tumorigenic processes. However, whether miR-129-2-3p is implicated in the ICC initiation and progression is still limited. Here, the results revealed that miR-129-2-3p expression was notably decreased in ICC tissues and cell lines, and that a low miR-129-2-3p expression was obviously associated with distant metastasis and clinical stage. Exogenous miR-129-2-3p expression evidently repressed the proliferative and invasive abilities of ICC cells. Mechanistic studies indicated that Wild-type p53-induced phosphatase 1 (Wip1) was a direct target gene for miR-129-2-3p in ICC cells. Furthermore, silencing Wip1 expression mimicked the suppressive effects of miR-129-2-3p upregulation on ICC cells. Interestingly, reintroduction of Wip1 expression partially abolished the miR-129-2-3p -reduced cell proliferation and invasion in ICC. Moreover, ectopic miR-129-2-3p expression hindered the ICC tumor growth in vivo. To the best of our knowledge, it is the first time to reveal that miR-129-2-3p plays a crucial role in tumor suppression in ICC pathogenesis through directly targeting Wip1. These results will aid in elucidating the roles of miR-129-2-3p in ICC, and suggest that this miRNA may provide a potential target for the treatment of ICC

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“…For instance, miR-182 16 , miR-30a 17 and miR-200c-3p 18 act as tumor suppressors to inhibit the progression of ccRCC by respectively targeting IGF1R, ADAM9 and SLC6A1, while miR-654 19 and miR-543 20 facilitate ccRCC cell proliferation and metastasis by targeting GK5 and Krüppel-like factor 6 (KLF-6), respectively. Generally speaking, miR-129-5p is considered to be a tumor suppressor and is down-regulated in prostate cancer (PC) 21 , bladder cancer (BC) 22 , etc. Wu Z et al pointed out that the long non-coding RNA SNHG12 acts as a competing endogenous RNA to regulate MDM4 expression by competing with miR-129-5p in ccRCC 12 .…”

Section: Discussionmentioning

confidence: 99%

miR-129-5p inhibits clear cell renal cell carcinoma cell proliferation, migration and invasion by targeting SPN

Gao

Wang

Zhang

et al. 2020

Preprint

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Objective: Our study aims to investigate the mechanism of the miR-129-5p/SPN axis in clear cell renal cell carcinoma (ccRCC), providing a novel direction for the targeted therapy of ccRCC. Methods: Bioinformatics methods were implemented to find the differentially expressed genes (DEGs) associated with ccRCC from TCGA database. qRT-PCR was performed to detect miR-129-5p and SPN mRNA expression, while western bot was carried out for the detection of protein expression of SPN. Bioinformatics analysis was used to predict the binding sites of miR-129-5p on SPN 3’UTR, while dual-luciferase assay was conducted to verify their binding relationship. CCK-8 assay, colony formation assay, wound healing assay and Transwell assay were employed to measure ccRCC cell proliferative ability, cell formation ability, cell migratory and invasive abilities. Results: miR-129-5p exhibited a significantly down-regulated expression level in ccRCC, while SPN showed a remarkably up-regulated expression level. Overexpressed miR-129-5p inhibited ccRCC cell proliferative, invasive and migratory capacities. Dual-luciferase assay confirmed that there was a binding relationship between miR-129-5p and SPN. Additionally, overexpressing miR-129-5p markedly reduced SPN expression in tumor cells, and attenuated the promoting effect of SPN on cell proliferation, migration and invasion. Conclusion: Our study proves the regulatory effect of the miR-129-5p/SPN axis in ccRCC, and provides a novel potential target for precise treatment of patients with ccRCC.

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<p>miR-129-5p inhibits prostate cancer proliferation via targeting ETV1</p>

Cited by 28 publications

References 44 publications

Chondrocyte suppression is mediated by miR‐129‐5p via GDF11/SMAD3 signaling in developmental dysplasia of the hip

Chondrocyte suppression is mediated by miR‐129‐5p via GDF11/SMAD3 signaling in developmental dysplasia of the hip

MicroRNA-129-2-3p directly targets Wip1 to suppress the proliferation and invasion of intrahepatic cholangiocarcinoma

miR-129-5p inhibits clear cell renal cell carcinoma cell proliferation, migration and invasion by targeting SPN

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