miR-129-5p Promotes Osteogenic Differentiation of BMSCs and Bone Regeneration via Repressing Dkk3

Zhao, Chang-Ming; Gu, Yulin; Wang, Yan; Qin, Qiaozhen; Wang, Ting; Huang, Meng‐Chuan; Zhang, Heyang; Qu, Yannv; Zhang, Jingwen; Du, Zhangzhen; Jiang, Xiaoxia; Xu, Lulu

doi:10.1155/2021/7435605

Cited by 23 publications

(15 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-129-5p, located on p13, functions as a tumor obstructor to restrain malignant behaviors of cancer cells. MiR-129-5p plays a critical role in bone development, and miR-129-5p has been confirmed to promoter the differentiation of bone marrow mesenchymal stem cells [ 9 ]. Moreover, several reports have indicated that aberrant abundance of miR-129-5p is associated with multiple bone diseases.…”

Section: Introductionmentioning

confidence: 99%

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

Chen

2022

Journal of Healthcare Engineering

View full text Add to dashboard Cite

Object. Rheumatoid arthritis (RA) is an osteoarticular disease which seriously affects the motor abilities of the patients. MicroRNA disorder has been confirmed as a biomarker event in RA development, and several studies have identified that miR-129-5p is related with the progression of multiple bone diseases. The study attempted to investigate the regulation mechanism of miR-129-5p in RA development. Methods. The abundance of miR-129-5p was detected in the samples including normal tissues and RA tissues and cell lines including human fibroblast-like synoviocytes (hFLSs) and human rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs). The CCK-8 assay, flow cytometry, Transwell, and ELISA were used to observe the effects of miR-129-5p on the phenotype of RA-FLSs. Moreover, the potential targets of miR-129-5p were identified with TargetScan and dual-luciferase reporter gene assay. Besides, the abundances of the proteins were analyzed with western blot. Results. Decreased miR-129-5p was observed in RA tissues and cells. Increased miR-129-5p obviously blocked the proliferation, inflammatory stress, and migration and remarkably promoted cellular apoptosis. Moreover, BRD4 was confirmed as targets of miR-129-5p, and BRD4 upregulation could partly rescue the inhibition of miR-129-5p on aggressive behaviors of RA-FLSs. Besides, the finding of this study also proved that upregulated miR-129-5p could impede the NF-κB pathway via targeting BRD4. Conclusion. This study suggests that miR-129-5p suppresses the activation of NF-κB pathway to block the progression of RA via targeting BRD4.

show abstract

Section: Introductionmentioning

confidence: 99%

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

Chen

2022

Journal of Healthcare Engineering

View full text Add to dashboard Cite

show abstract

“…Genepharma was procured for miRNA mimics and inhibitors (Shanghai, China). The vector, siRNA, miRNA mimics, and inhibitor were transfected into cells using lipofectamine 3000 (Thermo Fisher, USA) as previous study [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

“…The immunohistochemical staining was followed by several revisions to the previous study [ 21 ]. The formalin-fixed and paraffin-embedded tissue were deparaffinated and washed twice with PBS.…”

Section: Methodsmentioning

confidence: 99%

Lnc-SELPLG-2:1 enhanced osteosarcoma oncogenesis via hsa-miR-10a-5p and the BTRC cascade

Zeng

Yang

et al. 2022

BMC Cancer

View full text Add to dashboard Cite

Background To investigate the potential role of Long Non-coding RNAs (lncRNAs) in the progression of osteosarcoma. Methods The candidate lncRNAs were screened with RNA-seq and confirmed with quantitative real-time PCR. Using MTS, transwell assay, and flow cytometric analysis, the effects of overexpressed lnc-SELPLG-2:1 on cell functions were determined. Immunohistochemical staining, fluorescence in situ hybridization, and luciferase reporter assay were used to evaluate the potential mechanism of lnc-SELPLG-2:1 in vivo and in vitro using a tumor model. Moreover, the effects of overexpression of hsa-miR-10a-5p on the functions of SaOS2 cells were determined using functional cell analysis. A response test was used to confirm the mechanism by which lnc-SELPLG-2:1 sponge hsa-miR-10a-5p promotes the expression of BTRC to regulate osteosarcoma. Results Lnc-SELPLG-2:1 was highly expressed in osteosarcoma compared to normal cells and bone and marrow samples. Inhibition of lnc-SELPLG-2:1 accelerated cell apoptosis and suppressed cell proliferation, migration, and invasion, whereas lnc-SELPLG-2:1 overexpression had the opposite effect. Moreover, inhibiting lnc-SELPLG-2:1 in an in vivo model decreased tumor size and suppressed the expression of cell migration-related proteins. The prediction, dual luciferase assay, and response test results indicated that hsa-miR-10-5p and BTRC were involved in the lnc-SELPLG-2:1 cascade. Unlike lnc-SELPLG-2:1, hsa-hsa-miR-10a-5p had opposite expression and function. Competitive binding of lnc-SELPLG-2:1 to hsa-hsa-miR-10a-5p prevented BTRC from miRNA-mediated degradation, thereby activating the expression of VIM, MMP9, and MMP2, promoting osteosarcoma cell proliferation, migration, and invasion, and inhibiting apoptosis. Conclusion Lnc-SELPLG-2:1 is an oncogenesis activator in osteosarcoma, and its functions are performed via hsa-miR-10a-5p /BTRC cascade.

show abstract

“…Transfection of scramble control and OPRK1 siRNA (50 nM) (synthesized by GenePharma) in cells were performed according to the manufacturer’s instructions of Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro

Ma²,

Lei

2021

BMC Anesthesiol

View full text Add to dashboard Cite

Background Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown. Methods Small interfering RNA (siRNAs) was used to knockdown the expression of OPRK1. Western blot was used to determine the protein expression and reverse transcription-quantitative PCR (RT-qPCR) determined the genes transcription. Cell viability was detected by MTT assay and cell death rates were determined by Annexin V/PI and flow cytometry. Cell migration and invasion were detected by wound healing analysis and transwell assay, respectively. Results Our research demonstrated that OPRK1 was overexpressed in breast cancer cells compared with the normal human mammary epithelial cells. OPRK1 knockdown could inhibited cell viability and migration in cancer cells, accompanied with the decreased proteins and genes expression of N-cadherin, Snail, MMP2 and Vimentin, while the E-cadherin expression was increased. Additionally, OPRK1 knockdown also promoted PI3K/AKT signaling inactivation. Activation of AKT reversed the OPRK1 knockdown-induced cell viability inhibition and migration suppression, while inhibition of AKT reduced cell viability and promoted cell death. Conclusions Our findings illustrated the role of OPRK1 played on promoting migration in vitro, and we also provided the therapeutic research of OPRK1 knockdown combined with AKT inhibition.

show abstract

miR-129-5p Promotes Osteogenic Differentiation of BMSCs and Bone Regeneration via Repressing Dkk3

Cited by 23 publications

References 39 publications

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

Lnc-SELPLG-2:1 enhanced osteosarcoma oncogenesis via hsa-miR-10a-5p and the BTRC cascade

The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro

Contact Info

Product

Resources

About