This study aimed to investigate the key roles of miR-4286 in regulating the development of esophageal carcinoma, as well as its regulatory mechanism. The expression of miR-4286 in esophageal carcinoma tissues and cells was determined. Effects of abnormal expression of miR-4286 cell viability, apoptosis, migration and invasion were further investigated. Furthermore, the potential target of miR-4286 was explored, and the regulatory relationship between miR-4286 and Janus tyrosine kinase/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway was elucidated. The results showed that miR-4286 was highly expressed in esophageal carcinoma tissues and cells. Overexpression of miR-4286 significantly promoted cell viability, migration and invasion. In addition, Inositol Polyphosphate 4-Phosphatase Type I Gene (INPP4A) was a target of miR-4286. The effects of miR-4286 inhibitor on cell proliferation, migration, invasion and apoptosis were significantly counteracted by knockdown of INPP4A concurrently. Furthermore, inhibition of miR-4286 suppressed the activation of JAK2/STAT3 pathway, which was reversed after miR-4286 inhibition and INPP4A knockdown at the same time. Our findings reveal that highly expression of miR-4286 may promote the development of esophageal carcinoma by targeting INPP4A to evoke the JAK2/STAT3 pathway activation. miR-4286 may serve as a promising target for esophageal carcinoma treatment.