WNK1 facilitates cell proliferation, invasion and angiogenesis of gastric adenocarcinoma through AKT/VEGFA pathway through LINC00662/miR-103a-3p/WNK1 axis

Gastric adenocarcinoma (GAC) is a very familiar malignant tumor in human accompanied with higher mortality. With-no-lysine kinase 1 (WNK1) have been discovered to be a pivotal participator to aggravate the cancers’ progression. However, the regulatory effects of WNK1 on GAC development have not been investigated. The aim of this work is to study the functions of WNK1 in GAC progression. In this study, firstly, it was demonstrated that WNK1 exhibited higher expression, and GAC patients with higher WNK1 expression had poor prognosis. Overexpression of WNK1 facilitated, and knockdown of WNK1 suppressed cell proliferation, invasion and angiogenesis in GAC. Besides, WNK1 activated the AKT/VEGFA pathway. Moreover, the regulatory impacts of WNK1 knockdown on GAC cell proliferation, invasion and angiogenesis can be rescued after 740 Y-P treatment. Through in vivo assay, it was proved that WNK1 accelerated tumor growth in vivo. Further experiments demonstrated that LINC00662 sponged miR-103a-3p to target WNK1. Lastly, rescue assays uncovered that LINC00662/miR-103a-3p/WNK1 axis aggravated GAC progression. In conclusion, WNK1 facilitated cell proliferation, invasion and angiogenesis in GAC through AKT/VEGFA pathway through LINC00662/miR-103a-3p/WNK1 axis. Our findings illustrated that WNK1 may be one available bio-target for GAC treatment.