1. KNTC1 knockdown inhibits the proliferation and migration of osteosarcoma cells by MCM2.
- Author
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Zhong L, Dong Y, and Liu S
- Subjects
- Animals, Female, Humans, Male, Mice, Cell Line, Tumor, Mice, Inbred BALB C, Mice, Nude, Xenograft Model Antitumor Assays, Apoptosis genetics, Bone Neoplasms genetics, Bone Neoplasms pathology, Bone Neoplasms metabolism, Cell Movement genetics, Cell Proliferation genetics, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Minichromosome Maintenance Complex Component 2 genetics, Minichromosome Maintenance Complex Component 2 metabolism, Osteosarcoma pathology, Osteosarcoma genetics, Osteosarcoma metabolism
- Abstract
Osteosarcoma (OS) is a common primary malignant bone tumor, and it is necessary to further investigate the molecular mechanism of OS progression. The expression of kinetochore associated protein 1 (KNTC1) and minichromosome maintenance 2 (MCM2) was detected by immunohistochemistry, quantitative PCR (qPCR) and Western blot. Gene knockdown or overexpression cell models were constructed and the proliferation, apoptosis, cell cycle and migration were detected in vitro, besides, xenograft models were established to explore the effects of KNTC1 downregulation in vivo. Public databased and bioinformatics analysis were performed to screen the downstream molecules and determine the expression of MCM2 in cancers. KNTC1 was overexpressed in OS tissues and positively correlated with overall survival of OS patients. KNTC1 knockdown inhibited the proliferation and migration, and arrested G2 phase, and induced apoptosis. Besides, KNTC1 downregulation restricted the xenograft tumor formation. MCM2, one of the coexpressed genes, was highly expressed in sarcoma and downregulated after KNTC1 knockdown. MCM2 overexpression heightened the proliferation and migration ability of OS cells, which was reversed the inhibiting effects of KNTC1 knockdown. KNTC1 was overexpressed in OS and promoted the progression of OS by upregulating MCM2., (© 2024 Wiley Periodicals LLC.)
- Published
- 2024
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