Objective To determine the role of AAMP in osteosarcoma cells and explore the mechanism of invasion and metastasis of osteosarcoma cells regulated by AAMP through the YAP signaling pathway. Methods Public sequencing data analysis was used to explore the correlation between AAMP and osteosarcoma. q-PCR, Western blot, and immunohistochemistry were used to detect the expression levels of osteosarcoma cell-related molecules. CCK-8 was used to detect cell proliferation ability. Transwell and wound healing assays were used to detect the invasive and metastatic abilities of osteosarcoma cells. Immunofluorescence was used to detect the cell localization and expression levels of related molecules. Results High expression of AAMP was negatively correlated with the prognosis of patients with osteosarcoma (P<0.05), and the expression of AAMP in patients with metastatic osteosarcoma increased (P<0.05). Compared with the control group, the AAMP interference group showed significantly decreased migratory, invasive, and EMT activities (P<0.05). The expression of p-CFL1 reduced after the knockdown of AAMP, and the cell plate pseudopods decreased significantly (P<0.05). A positive correlation was found between the expression levels of AAMP and YAP in osteosarcoma cells (P<0.05). Interfering with YAP expression can affect the migration and invasion of osteosarcoma cells. Conclusion AAMP promotes osteosarcoma cell metastasis by regulating the YAP signaling pathway, suggesting that AAMP may be a key molecule in promoting invasion and metastasis of osteosarcoma.

Metastasis is crucial for the mortality of non-small cell lung carcinoma (NSCLC) patients. The epithelial-mesenchymal transition (EMT) plays a critical role in regulating tumor metastasis. Glioma-associated oncogene 1 (Gli1) is aberrantly active in a series of tumor tissues. However, the molecular regulatory relationships between Gli1 and NSCLC metastasis have not yet been identified. Herein, we reported Gli1 promoted NSCLC metastasis. High Gli1 expression was associated with poor survival of NSCLC patients. Ectopic expression of Gli1 in low metastatic A549 and NCI-H460 cells enhanced their migration, invasion abilities and facilitated EMT process, whereas knock-down of Gli1 in high metastatic NCI-H1299 and NCI-H1703 cells showed an opposite effect. Notably, Gli1 overexpression accelerated the lung and liver metastasis of NSCLC in the intravenously injected metastasis model. Further research showed that Gli1 positively regulated Snail expression by binding to its promoter and enhancing its protein stability, thereby facilitating the migration, invasion and EMT of NSCLC. In addition, administration of GANT-61, a Gli1 inhibitor, obviously suppressed the metastasis of NSCLC. Collectively, our study reveals that Gli1 is a critical regulator for NSCLC metastasis and suggests that targeting Gli1 is a prospective therapy strategy for metastatic NSCLC.