Heat shock protein gp96 is overexpressed in many kinds of tumors including hepatic tumors, and its overexpression is significantly correlated with tumor malignant degree and poor prognosis in patients. The mechanisms of heat shock protein gp96 in the development of tumors need to be further investigated. The effects of gp96 3′UTR as a ceRNA (competing endogenous RNA) on miR-642a and DOHH expression was studied through bioinformatics prediction, luciferase reporter assay, Western blotting, real-time PCR, RNA interference. MiR-642a specifically targets gp96 3′UTR. The wild type but not the mutant gp96 3′UTR in miR-642a binding site could sequester and downregulate miR-642a levels, which led to increased expression of the miR-642a target DOHH. Further studies showed that regulation of DOHH expression by gp96 3′UTR was miR-642a dependent. It was also found that DOHH does not affect the expression of gp96. Heat shock protein gp96 promotes DOHH expression via its 3′UTR as a ceRNA, providing new insights into the role of gp96 on the development of hepatic tumors and other tumors.