Jinyu Zhang,1 Xiang Ma,1 Ruiqi Zhou,1 Yichi Zhou2 1Department of Orthopaedics, The Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming 650118, People's Republic of China; 2Department of Orthopaedics, CR & WISCO General Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, Hubei 430000, People's Republic of ChinaCorrespondence: Yichi ZhouCR & WISCO General Hospital Affiliated to Wuhan University of Science and Technology, No.

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... 9 Yejin Avenue, Qingshan District, Wuhan, Hubei 430000, People's Republic of ChinaEmail zhouyichi26@126.comIntroduction: The yes-associated protein (YAP) and trichorhinophalangeal syndrome 1 (TRPS1) have been reported to account for the pathogenesis of cancers and may play an important role in osteosarcoma (OS). This study intended to investigate the modulatory effect and relationship of TRPS1 and YAP1 in OS cells.Methods: The expression difference of YAP1 and TRPS1 in OS cells was measured. Then, the effect of circTADA2A silence on YAP1 and TRPS1 expression as well as OS proliferation and drug resistance was estimated.Results: TRPS1 and YAP1 were upregulated in OS cell lines, and TRPS1 and YAP1 were highly expressed in MG63 and U2OS cells, respectively. The cell proliferation of MG63 was lower than that of U2OS, but the opposite result was observed in the presence of cisplatin (DDP). CircTADA2A was upregulated while miR-129-5p was downregulated in MG63 and U2OS cells compared. Besides, circTADA2A knockdown inhibited cell proliferation and reduced DDP resistance in both MG63 and U2OS. MiR-129-5p was increased but TRPS1 and YAP1 were decreased by circTADA2A knockdown. Meanwhile, circTADA2A knockdown reduced TRPS1 protein expression but enhanced phosphorylated (p)-YAP1. In xenograft OS tumor mice, circTADA2A knockdown inhibited tumor growth in the absence or presence of DDP. Finally, miR-129-5p could bind to circTADA2A, TRPS1 and YAPS.Discussion: CircRNA TADA2A could target miR-129-5p, which was competitively bound by TRPS1 [...]