Knockdown of FSCN1 impaired cell proliferation, migration and invasion in osteosarcoma by manipulating epithelial-mesenchymal transition
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刊名 Journal of Advances in Basic Medicine
作者 Qiang Sun1, Ran Liang2, Mingdong Li3, Hua Zhou3,* 英文名 Electronic Communication Technology 年,卷(期) 2025年,第1期
主办单位 睿核出版社有限公司 刊号 DOI

Knockdown of FSCN1 impaired cell proliferation, migration and invasion in osteosarcoma by manipulating epithelial-mesenchymal transition

Background: Osteosarcoma is the most common primary malignant tumor initially in bone with multiple genomic aberrations. Fascin-1 (FSCN1) is a cytoskeletal protein link with the progression of diverse tumors. However, its function in osteosarcoma is not understand completely. Materials and Methods: The expression arrays in osteosarcoma tissues were obtained from Gene Expression Omnibus (GEO) database and analyzed by GEO2R, the expression level of FSCN1 in osteosarcoma cell lines was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) . The effects of FSCN1 were examined on cell growth, colony formation ability, cell migration and invasion in MG-63 cells after knockdown FSCN1 through some vitro experiments, such as Cell Counting Kit 8 (CCK 8) assay, colony formation and transwell methods. Furthermore, the western blot was used to study the influence of FSCN1 on epithelial-mesenchymal transitions (EMT). Results: Our results indicated that when compared with normal tissues and cells, FSCN1 was promoted obviously in osteosarcoma tissues and cells. High expression of FSCN1 could lead to a poor prognosis in patients with osteosarcoma. And cell proliferation, colony formation ability, migration and invasion were blocked because of reduced FSCN1 in vitro. Moreover, E-cadherin expression was induced while N-cadherin, Vimentin, Snail1 and Snail2 were inhibited. Conclusions: In conclusion, the findings revealed that FSCN1 facilitates osteosarcoma EMT and sheds new insights into osteosarcoma targeted therapy.

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