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Research Paper Volume 12, Issue 23 pp 23598—23608
Exosome-mediated Hic-5 regulates proliferation and apoptosis of osteosarcoma via Wnt/β-catenin signal pathway
- 1 Department of Orthopedics, People’s Hospital of Rizhao, Rizhao 276826, Shandong Province, China
Received: March 3, 2020 Accepted: June 4, 2020 Published: December 13, 2020
https://doi.org/10.18632/aging.103546How to Cite
Copyright: © 2020 Sha et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The expression of Hic-5 was detected in osteosarcoma patients and osteosarcoma cell lines by RT-PCR. Then RFP-sh-Hic-5 was transfected into osteosarcoma cell lines. The effect of Hic-5 on cell viability, proliferation and apoptosis were assessed by MTT, EdU kit and Flow cytometry. The exosomes were isolated from MG-63 cell supernatant by an Exosome Isolation Kit. The exosome-Hic-5 was confirmed by transmission electron microscope, particle size detection and RT-PCR. Next, exosome-Hic-5 treated cells were explored the cell viability, proliferation and apoptosis. Further, Co-IP assay was employed for identifying the relationship between Hic-5 and smad4. TCF/LEF and the protein level of components of wnt/β-catenin signals were detected by TOP luciferase assay and western blot. Hic-5 was upregulated in osteosarcoma tissues and cell. Forced decreased expression Hic-5 inhibited the proliferation of osteosarcoma cell lines, and induced apoptosis of MG-63 and HOS. In vivo, silencing Hic-5 remitted the tumor progression. Further, we isolated the exosomes from MG-63 supernatant, exosomes concluding Hic-5 would regulated the proliferation and apoptosis level of MG-63 and HOS cells. Further, Hic-5 interacted with smad4 and regulated Wnt/β-catenin signal by decreasing TCF/LEF activity. Silencing Hic-5 inhibited the proliferation and induced apoptosis of osteosarcoma cell via inactivating Wnt/β-catenin signal by exosome pathway.