miR-486 suppresses the development of osteosarcoma by regulating PKC-δ pathway

He, Ming; Wang, Guangbin; Jiang, Linlin; Qiu, Chuang; B, Li; Wang, Jiashi; Fu, Yue

doi:10.3892/ijo.2017.3928

Cited by 30 publications

(23 citation statements)

References 32 publications

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“…For instance, miR-486-5p could act as an anti-oncogene and biomarker in non-small cell lung cancer (NSCLC), inhibiting the development and growth of NSCLC in mouse models 27, 28. The level of miR‑486 is low in osteosarcoma and patients who have low expression of miR-486 possess shorter median survival than those with higher miR‑486 29. Consistent with previous findings, it was discovered that miR-486-5p level was markedly reduced in breast cancer tissues than corresponding ANTs, thus miR-486-5p played as anti-oncogene in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1

Liu

Mou

et al. 2019

J. Cancer

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Epithelial-mesenchymal transition (EMT) is one of important steps that lead to cancer metastasis. Interleukin-22 (IL-22) is a T helper 17 (Th17) cells-secreted cytokine, it can promote invasion and metastasis of many cancers. MiR-486-5p is a microRNA that known to function as a tumor suppressor, and bioinformatics analysis predicts that Dock-1 has a binding site of miR-486-5p. In current research, we examined the relative expression levels of miR-486-5p and Dock-1 in 80 pairs of breast cancer tissues and corresponding adjacent normal tissues, also the effects of modifying their levels in cultured cells. We illustrated that IL-22 and Dock1 promote the invasion, metastasis, and EMT of breast cancer using Transwell invasion assay, western blot and immunofluorescence. MiR-486-5p directly bound the Dock1 mRNA 3' untranslated region and inhibited IL-22-induced EMT of breast cancer cells via the Dock1/NF-κB/Snail signaling pathway. Dock1 overexpression reversed the effect caused by the overexpression of miR-486-5p. Overexpression of miR-486-5p or downregulation of Dock1 reduced pulmonary metastasis in mice. This study provided insight into a potential mechanism where miRNAs regulate breast cancer metastasis and provided a novel therapeutic target for breast cancer treatment.

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Section: Discussionmentioning

confidence: 99%

MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1

Liu

Mou

et al. 2019

J. Cancer

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“…For osteosarcoma, another lncRNA-ATB promotes proliferation, migration, and invasion depending on the regulation of miR-200s [ 29 ]. In osteosarcoma tissue, miR-486 was down-regulated, and further found that miR-486 inhibited the targeting of PKC-δ signaling pathways, and ulteriorly inhibit the growth and invasion of osteosarcoma cells [ 30 ]. In prostate cancer tissue and cells, miR-486-5p sponged Snail, a key regulator of the epithelial-mesenchymal transition, to suppress cell migration and the invasive ability [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA ZFAS1 sponges miR-486 to promote osteosarcoma cells progression and metastasis in vitro and vivo

Sun

Fang

et al. 2017

Oncotarget

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Long noncoding RNAs (lncRNAs) have been wildly demonstrated to participate in the osteosarcoma tumorigenesis. ZFAS1 is a novel identified lncRNA, however, its role in osteosarcoma is still unclear. In present study, we utilize lncRNA microarray assay to screen the lncRNA expression profile in osteosarcoma tissue, and investigate the regulatory function of ZFAS1 in osteosarcoma. LncRNA microarray assay revealed that lncRNA ZFAS1 was significantly up-regulated in 3 pairs of osteosarcoma and adjacent non-tumor tissue, which was confirmed by RT-PCR. Furthermore, in 53 pairs of osteosarcoma patient samples, the up-regulated expression of ZFAS1 was closely related to poor prognosis. In vitro, loss-of-function experiments showed that ZFAS1 knockdown significantly suppressed the proliferation, induced cycle arrest at G0/G1 phase and enhance apoptosis. In vivo, ZFAS1 knockdown inhibited the tumor growth. Bioinformatics online programs predicted that ZFAS1 sponge miR-486 at 3’-UTR with complementary binding sites, which was validated using luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Rescue experiments confirmed that miR-486 could reverse the functions of ZFAS1 on osteosarcoma genesis. In conclusion, our results demonstrate that ZFAS1 act as competing endogenous RNA (ceRNA) for miR-486, and act as oncogene in osteosarcoma tumorigenesis, and discover the functional regulatory pathway of ZFAS1 sponging miR-486.

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“…Moreover, many studies revealed that miRNAs played vital roles in OS. For example, miR-486 suppressed proliferation and migration of OS [21]. And miR-504 facilitated growth and migration in OS [22].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: The circular RNA circ-ITCH acts as a tumour suppressor in osteosarcoma via regulating miR-22

Ren

Liu

Zheng

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Osteosarcoma (OS) is the most prevailing primary bone tumour and the third prevalent tumour in children and adolescents. Despite advanced treatments, the survival rate of OS has not been effectively improved. Here, we intended to investigate the functional impacts of circ-ITCH on OS. Methods: Circ-ITCH expression in OS tissues and cells was evaluated utilizing qRT-PCR. Viability and proliferation of MG63 and Saos-2 cells were determined by utilizing CCK-8 assay and BrdU assay. Transwell assay was utilized to investigate migration and invasion. Western blot was utilized to distinguish apoptosis and metastasis-related proteins expression. Sequentially, the above-mentioned parameters were reassessed when up-regulating miR-22. Results: Circ-ITCH was low expressed in OS tissues and cells. Overexpressing circ-ITCH facilitated apoptosis and repressed viability, proliferation, migration and invasion in MG63 and Saos-2 cells. MiR-22 expression was reduced by overexpressing circ-ITCH. The decline of viability, proliferation, migration and invasion made by overexpressing circ-ITCH was alleviated by up-regulating miR-22. Conclusively, circ-ITCH suppressed PTEN/PI3K/AKT and SP-1 pathways via down-regulating miR-22. Conclusion: Circ-ITCH took effects on apoptosis, viability, proliferation, migration and invasion through restraining PTEN/PI3K/AKT and SP-1 pathways via down-regulating miR-22 in MG63 and Saos-2 cells. HIGHLIGHTS 1. Low expression of circ-ITCH is observed in osteosarcoma tissues and cell lines; 2. Overexpression circ-ITCH suppresses miR-22 expression; 3. Circ-ITCH promotes proliferation and represses apoptosis by up-regulating miR-22; 4. Circ-ITCH promotes migration and invasion by up-regulating miR-22; 5. Circ-ITCH activates PTEN/PI3K/AKT and SP-1 pathways by up-regulating miR-22.

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miR-486 suppresses the development of osteosarcoma by regulating PKC-δ pathway

Cited by 30 publications

References 32 publications

MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1

MiR-486-5p inhibits IL-22-induced epithelial-mesenchymal transition of breast cancer cell by repressing Dock1

Long non-coding RNA ZFAS1 sponges miR-486 to promote osteosarcoma cells progression and metastasis in vitro and vivo

RETRACTED ARTICLE: The circular RNA circ-ITCH acts as a tumour suppressor in osteosarcoma via regulating miR-22

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