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Background  Fibroblast growth factor (FGF) and tumor growth factor-β (TGFβ) have emerged as pivotal regulators during the progression of osteosarcoma (OS). LHX9 is one crucial transcription factor controlled by FGF, however, its function in OS has not been investigated yet.    Methods  The expression of  LHX9 ,  FRS2 ,  BMP4 ,  TGF - beta R1 ,  SMAD2 ,  beta - catenin  and metastasis-related proteins was measured by real-time quantitative PCR (RT-qPCR) and Western blot. CCK-8 assay and colony formation assay were employed to determine the proliferation of OS cells, while scratch wound healing assay and transwell assay were used to evaluate their migration and invasion, respectively. In vivo tumor growth and metastasis were determined by subcutaneous or intravenous injection of OS cells into nude mice.    Results   LHX9  expression was evidently up-regulated in OS tumor tissues and cell lines. Knockdown of  LHX9  impaired the proliferation, migration, invasion and metastasis of OS cells. Mechanistically,  LHX9  silencing led to the down-regulation of BMP-4, β-catenin and metastasis-related proteins, which was also observed in  beta - catenin  knockdown OS cells. By contrast,  FRS2  knockdown conduced to the up-regulation of  LHX9 , BMP4, β-catenin and TGF-βR1, while  TGF - beta  inhibition repressed the expression of  LHX9  and metastasis-related proteins. Additionally,  let - 7c  modulates  LHX9  and metastasis-related proteins by suppressing TGF- beta  R1 expression on transcriptional level.    Conclusions  This study revealed  LHX9  was essential for the proliferation, migration, invasion, and metastasis of OS cells via FGF and TGF-β/β-catenin signaling pathways.

FGF-induced LHX9 regulates the progression and metastasis of osteosarcoma via FRS2/TGF-β/β-catenin pathway