LncRNA JPX Promotes Esophageal Squamous Cell Carcinoma Progression by Targeting miR-516b-5p/VEGFA Axis

Simple Summary LncRNA JPX acts as an oncogenic regulator in various types of cancer. Here, we present insights into the mechanistic evidence for the function of JPX in ESCC progression. To clarify the potential role of JPX in ESCC, JPX was upregulated or downregulated in ESCC cells, and in a xenograft model. We showed that JPX promoted ESCC cell proliferation, migration, and invasion via the miR-516b-5p/VEGFA pathway. Our study revealed the importance of JPX as a promising biomarker for ESCC diagnosis and therapeutic target for ESCC in clinic. Long non-coding RNAs (lncRNAs) are reported act as important regulators in various types of cancer. LncRNA JPX was identified as an oncogenic regulator in lung cancer. However, the function of JPX in the progression of esophageal squamous cell carcinoma (ESCC) remains unclear. In the present study, we found JPX was highly expressed in esophageal tissue from ESCC patients. Functional assays demonstrated that JPX promoted ESCC cell proliferation, migration, and invasion in vitro, and accelerated tumor growth in vivo. Mechanistically, the results showed that JPX functioned as a sponge of miR-516b-5p, which targeted vascular endothelial growth factor A (VEGFA) in ESCC cells. Interactions between miR-516b-5p and JPX or VEGFA were confirmed by luciferase reporter assays. Inhibition of JPX significantly attenuated the cell growth and mobility ability of ESCC cells in vitro. In addition, overexpression of miR-516b-5p abrogated JPX-enhanced proliferation, migration, invasion, and angiogenesis of ESCC cells. Our study demonstrated that JPX played an important role in promoting ESCC progression via the miR-516b-5p/VEGFA pathway, which might serve as a promising novel diagnostic biomarker and therapeutic target for ESCC in clinic.