Conclusion
BAIAP2L2 is upregulated in gastric cancer, and knockdown of BAIAP2L2 inhibited the proliferation and metastasis through the inactivation of AKT/mTOR and Wnt3a/β-catenin signaling pathways.
Methods
BAIAP2L2 expression was analyzed via online database and immunohistochemistry. The proliferation was detected using CCK8 and colony formation assay. The migration and invasion was confirmed by transwell assay, and the apoptosis of gastric cancer cells was detected by flow cytometry.
Results
BAIAP2L2 was highly expressed in tumour tissues and its expression significantly correlated with tumor diameter, T stage, pTNM stage and lymph node metastasis, respectively. Compared with GES-1 cells, SGC7901, MKN28, MKN45, AGS and BGC-823 tumor cells were all presented a high-expression of BAIAP2L2. The in vitro results showed that knockdown of BAIAP2L2 inhibited the proliferation, migration and invasion, and induced the apoptosis of gastric cancer cell. Further, knockdown of BAIAP2L2 inhibited the expression of the related proteins of AKT/mTOR and Wnt3a/β-catenin signaling pathways.