miR-532-3p inhibits osteogenic differentiation in MC3T3-E1 cells by downregulating ETS1

Fan, Qingxin; Li, Yuqiao; Sun, Qiang; Jia, Yutao; He, Chao; Sun, Tianwei

doi:10.1016/j.bbrc.2020.02.126

Cited by 29 publications

(19 citation statements)

References 24 publications

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“…MiR-532-3p plays an important part in a variety of diseases [37]. Jiang et al showed that miR-532-3p inhibited the proliferation, invasion and migration of NSCLC cells through FOXP3 [38].…”

Section: Discussionmentioning

confidence: 99%

LINC00963 affects the development of colorectal cancer via MiR-532-3p/HMGA2 axis

Liu

Tang

et al. 2021

Cancer Cell Int

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Background LINC00963 is high-expressed in various carcinomas, but its expression and function in colorectal cancer (CRC) have not been explored. This study explored the role and mechanism of LINC00963 in CRC. Methods The expression of LINC00963 in CRC and its relationship with prognosis were examined by starBase and survival analysis. The effects of LINC00963, miR-532-3p and HMGA2 on the biological characteristics and EMT-related genes of CRC cells were studied by RT-qPCR, CCK-8, clone formation experiments, flow cytometry, scratch test, Transwell, and Western blot. Xenograft assay and immunohistochemistry were performed to verify the effect of LINC00963 on tumor growth. The correlation among LINC00963, miR-532-3p, and HMGA2 was analyzed by bioinformatics analysis, luciferase assay, and Pearson test. Results LINC00963 was high-expressed in CRC, and this was associated with poor prognosis of CRC. Silencing LINC00963 inhibited the activity, proliferation, migration, and invasion of CRC cells, MMP-3 and MMP-9 expressions, moreover, it also blocked cell cycle progression, and inhibited tumor growth and Ki67 expression. However, overexpression of LINC00963 showed the opposite effects to silencing LINC00963. LINC00963 targeted miR-532-3p to regulate HMGA2 expression. Down-regulation of miR-532-3p promoted cell proliferation, migration and invasion, and expressions of MMP-3 and MMP-9, and knockdown of HMGA2 reversed the effect of miR-532-3p inhibitor. Up-regulation of miR-532-3p inhibited the biological functions of CRC cells, and overexpression of HMGA2 reversed the miR-532-3p mimic effect. Conclusion LINC00963 affects the development of CRC through the miR-532-3p/HMGA2 axis.

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“…MiR-532-3p plays an important part in a variety of diseases [37]. Jiang et al showed that miR-532-3p inhibited the proliferation, invasion and migration of NSCLC cells through FOXP3 [38].…”

Section: Discussionmentioning

confidence: 99%

LINC00963 affects the development of colorectal cancer via MiR-532-3p/HMGA2 axis

Liu

Tang

et al. 2021

Cancer Cell Int

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“…In addition, it has been suggested that miRNAs are involved in the occurrence of bone diseases, such as osteoporosis ( 35 ), osteoarthritis ( 36 ), and osteosarcoma ( 37 ). For example, Fan et al ( 38 ) demonstrated that miR-532-3p attenuated osteogenic differentiation by downregulating ETS-1. Additionally, Xiaoling et al ( 39 ) previously reported that the upregulation of miR-19b-3p could promote osteogenic differentiation in BMSCs.…”

Section: Discussionmentioning

confidence: 99%

LINC00899 promotes osteogenic differentiation by targeting miR‑374a and RUNX2 expression

2021

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Accumulating researches indicate that long non-coding RNAs (lncRNAs) participate in human bone mesenchymal stem cells (hBMSCs) osteogenic differentiation. The present study aimed to investigate the underlying molecular mechanisms of long intergenic non-protein coding RNA 899 (LINC00899) in osteoporosis. Therefore, reverse transcription-quantitative PCR was performed to evaluate the expression levels of LINC00899, microRNA (miR)-374a and runt-related transcription factor 2 (RUNX2) in clinical tissues and hBMSCs. The potential interaction between miR-374a and LINC00899 or RUNX2 was predicted utilizing the StarBase software and verified by luciferase reporter and RNA binding protein immunoprecipitation assays. In addition, alkaline phosphatase activity and Alizarin Red S staining were used to evaluate the osteogenic potential of hBMSCs. The results showed that the expression levels of LINC00899 were gradually increased, whilst those of miR-374a were decreased as the osteogenic induction process progresses. Additionally, the expression of LINC00899 was downregulated in the bone tissues of patients with osteoporosis, where LINC00899 knockdown reduced the expression levels of osteogenesis-related genes osteocalcin (OCN), osteopontin (OPN) and RUNX2 in hBMSCs. LINC00899 was also found to directly target miR-374a, thereby inhibiting its expression. Finally, it was predicted that RUNX2 could be directly targeted by miR-374a, such that miR-374a silencing partially abolished the inhibitory effect of LINC00899 knockdown on the expression of RUNX2, OPN and OCN. Overall, findings of the present study suggested that LINC00899 could facilitate the osteogenic differentiation of hBMSCs and prevent osteoporosis by sponging miR-374a to enhance the expression of RUNX2, which provide a potentially useful therapeutic strategy for patients with osteoporosis.

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“…In addition, miRNAs have been reported to be involved in the occurrence of bone metabolic diseases [22]. For instance, Fan et al identi ed that miR-532-3p attenuated osteogenic differentiation by downregulating ETS1 [23]. Gan et al reported that miR-19b-3p promoted osteogenic differentiation of BMSCs [24].…”

Section: Discussionmentioning

confidence: 99%

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

Gao

Xue

Yang

2020

Preprint

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Objective: This study aims to illustrate the underlying molecular mechanisms of long noncoding RNAs (LncRNAs) LINC00899 in osteoporosis.Methods: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) used to examine the levels of LINC00899, miR-374a and RUNX2 in clinical tissues or human bone mesenchymal stem cells (hBMSCs). The interaction between miR-374a and LINC00899 or RUNX2 was predicted by starBase and verified by luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. Results: The expression of LINC00899 was lowly expressed in osteoporotic patients’ bone tissues and knockdown of LINC00899 decreased the expression of osteogenesis-related genes. Moreover, LINC00899 was confirmed to inhibit miR-374a expression by direct interaction. the expression levels of LINC00899 were gradually increased, but miR-374a expression was decreased with the prolongation of osteogenic induction. Finally, we demonstrated that RUNX2 was a target of miR-374a, and the silencing of miR-374a partially abolished the inhibitory effect of LINC00899 knockdown on the expression of RUNX2, OPN and OCN.Conclusions: We demonstrated that LINC00899 facilitated osteogenic differentiation of hBMSCs and prevent osteoporosis by sponging miR-374a and enhancing RUNX2 expression, which might provide a useful therapeutic strategy for osteoporosis patients.

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miR-532-3p inhibits osteogenic differentiation in MC3T3-E1 cells by downregulating ETS1

Cited by 29 publications

References 24 publications

LINC00963 affects the development of colorectal cancer via MiR-532-3p/HMGA2 axis

LINC00963 affects the development of colorectal cancer via MiR-532-3p/HMGA2 axis

LINC00899 promotes osteogenic differentiation by targeting miR‑374a and RUNX2 expression

LINC00899 Promotes Osteogenic Differentiation and Alleviates Osteoporosis via Targeting miR-374a to Regulate RUNX2

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