Open Access

ARTICLE

CDK5 inhibition promotes osteoblastic differentiation of MSCs and blocks the migration of osteosarcoma MG-63 cells

HONG FU¹, HAOYU ZHAO¹, YALI YANG¹, SIYU WANG¹, KE DUAN^2,*, TAILIN GUO^1,*

1 College of Medicine, Southwest Jiaotong University, Chengdu, 610031, China
2 Provincial Laboratory of Orthopaedic Engineering, Department of Bone and Joint Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China

* Corresponding Authors: KE DUAN. Email: ; TAILIN GUO. Email:

BIOCELL 2022, 46(4), 1067-1078. https://doi.org/10.32604/biocell.2022.017435

Received 10 May 2021; Accepted 07 July 2021; Issue published 15 December 2021

Abstract

CDK5 belongs to the cyclin-dependent kinase family. CDK5 is multifunctional and plays an important role in neural differentiation. However, the role of CDK5 in osteoblastic differentiation remains unclear. The present study investigated functions and molecular mechanism of CDK5 in osteoblastic differentiation. It was found that, CDK5 inhibition promoted the expression of Runx2, ALP, OCN and OPN of MSCs and the mineralization of MC-3T3E1 cells and MSCs. CDK5 inhibition enhanced the development of F-actin, nuclear localization of β-catenin and YAP, as well as the expression of RMRP RNA. When F-actin was suppressed by Blebbistatin, the nuclear localization of YAP and β-catenin, and expression of RMRP RNA as well as Runx2 and ALP were decreased. These indicate Seliciclib promotes osteoblastic differentiation mainly by F-actin. Moreover, Seliciclib also suppressed the migration of MG-63, suggesting a potential application for Seliciclib in bone defect repair and inhibition of the migration of osteosarcoma cells after osteosarcoma surgical resection.

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