Abstract
Esophageal squamous cell carcinoma (ESCC) is the major type of esophageal carcinoma, one of the main reasons of cancer-caused death. While the therapeutic effect on ESCC patents is still unsatisfactory as a result of tumor aggression, recurrence and metastasis. RNA-binding proteins, microRNAs and specific genes get involved in tumorigenesis and development of tumors in a large proportion. In several reports, SEMA4D is an oncogene and miR-4319 is a tumor suppressor. We discovered the interaction of SEMA4D with HuR and miR-4319, whereas the detailed mechanism in ESCC was yet to be researched. At first, SEMA4D was significantly overexpressed in ESCC cells, and its knockdown repressed cell proliferation and migration as well as accelerated cell apoptosis. And then HuR was proved to stabilize SEMA4D mRNA by binding to its 3'UTR. In addition, miR-4319 targeted and degraded SEMA4D. Taken together, SEMA4D was regulated competitively by HuR and miR-4319. Collectively, HuR and miR-4319 co-regulating SEMA4D affected cell proliferation, apoptosis and migration in ESCC. This research explored the regulatory mechanism on SEMA4D in ESCC and provided optional therapeutic targets for ESCC patients.