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MPP8 Promotes Proliferation and Restrains Apoptosis in Osteosarcoma by Regulating p38αMAPK Pathway
Author(s) -
Tao Li,
Na Li,
Lei Wang,
Jia Li,
Xin Zhang
Publication year - 2021
Publication title -
technology in cancer research and treatment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.754
H-Index - 63
eISSN - 1533-0346
pISSN - 1533-0338
DOI - 10.1177/1533033821995272
Subject(s) - osteosarcoma , cell growth , apoptosis , cancer research , gene knockdown , mapk/erk pathway , carcinogenesis , microbiology and biotechnology , transfection , p38 mitogen activated protein kinases , small hairpin rna , downregulation and upregulation , cell , cell culture , biology , chemistry , signal transduction , cancer , gene , genetics
Osteosarcoma is the most common primary bone malignancy. We aim to investigate that role of M-phase phosphoprotein 8 (MPP8) on proliferation and apoptosis in osteosarcoma. Briefly, the current research reported an in vitro study investigating the role MPP8 in OS tumorigenesis. Consequently, we found that the MPP8 expression was upregulated in osteosarcoma tissues and in osteosarcoma cell lines. Interestingly, MPP8 knockdown via shRNA restrained the cell viability and proliferation of U2OS and Saos-2 cells. In addition, MPP8 knockdown promoted the apoptosis of U2OS and Saos-2 cells, while MPP8 overexpression promotes proliferation and inhibited the cell apoptosis of osteosarcoma cells. These results suggested that MPP8 may serve as a contributor for osteosarcoma growth and inhibition of MPP8 may help restrain the development of osteosarcoma. Importantly, we found that MPP8 overexpression suppressed the protein levels of HOXA5, p38αMAPK, increased cell proliferation and inhibited cell apoptosis, while co-transfection with HOXA5 overexpression suppressed the cell proliferation and increased cell apoptosis. These results indicated that MPP8 contributed to cell proliferation and the underlying mechanism might be involved with HOXA5/ p38αMAPK pathway.

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