Objective To investigate mechanism of overexpression of long noncoding RNA MT1JP in inhibiting proliferation and invasion of retinoblastoma SORB50 cells and growth of transplanted tumors. Methods The retinoblastoma SORB50 cells were cultured in vitro and divided into Blank control group (control), transfection control group (Vector) and overexpression group (MT1JP). RT-PCR was performed to detect expression of MT1JP in each group. The growth of SORB50 cells was detected by colony formation. The apoptosis was detected by flow cytometry. The cell invasion was detected by Transwell. The expression of Ki67 and VEGF protein was detected by Western blot. SORB50 cells were subcutaneously injected into mice. The transplanted tumor model was established. The expression of long chain was detected by RTPCR. The survival time of nude mice was statistically analyzed. The survival curve was drawn. The tumor weight of mice was detected. The expression of Ki67 and VEGF in mice tumor tissues was detected by immunohistochemistry.〖WTHZ〗Results 〖WTBZ〗 Compared with the blank control group, there was no significant change in MT1JP expression, number of cell invasion per unit area, Ki67 or VEGF protein expression in transfection control group (P＞0.05). Compared with transfection control group, MT1JP expression and apoptosis rate in overexpression group were significantly increased (P＞0.05), while cell formation rate of cloning experiment, Ki67, VEGF protein expression and number of cell invasion per unit area were significantly decreased (P＜0.05). Compared with blank control group, there was no significant difference in tumor mass, survival time, Ki67 or VEGF protein expression in transfection control group (P＞0.05). Compared with transfection control group, MT1JP expression and survival in overexpression group were significantly increased (P＜0.05), while tumor mass, Ki67 and VEGF protein expression were significantly decreased (P＜0.05).Conclusion Overexpression of long noncoding RNA MT1JP can inhibit proliferation and invasion of retinoblastoma SORB50 cells, promote apoptosis of SORB50 cells and inhibit growth of transplanted tumors.