Background: MicroRNAs (miRNAs) are noncoding RNAs that control the expression of their target mRNAs. It affects cancer cell proliferation and apoptosis as oncogenes or tumor suppressors. Dysregulation of miRNAs expression leads to the development of various cancers. Therefore, for the first time in this field, this study investigated the effect of overexpression of microRNA-630 on the Jurkat cells. Materials and methods:: In this experimental study, the Jurkat cells were divided into the four groups, i.e. non-transfected control group (A), scramble (B), transfected with 50 nM concentrations of miR-630 (C), and treated with 100 nM miR-630 (D). MiR-630 transfection was performed by lipofectamine 2000. Cancer cell growth in each group was analyzed with MTT assay. Flow cytometry investigated percent of viable, necrotic, and apoptotic cells. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) measured the expression of P53, P21, and BCL2 genes. SPSS (version 21) especially Kruskal-Wallis and Mann-Whitney U tests were utilized for data analysis. Results: The results of MTT assay showed that the cell growth rates in C (118%) and D (136%) groups were significantly higher than that in the control group (P= 0.037 vs. 0.034). The percentage of early and late apoptosis in C (3.1% P=0.01, 4.2% P=0.02) and D (0.5% P=0.008, 0.4% P=0.006) groups were significantly lower than those in the control group. The expression of p53 and p21 in C (0.7 P=0.037, 0.62 P=0.034) and D (0.44 P=0.034, 0.53 P=0.038) Groups were significantly decreased compared with the control group. The expression of B-cell lymphoma-2 (Bcl2) in C (1.85) and D (3.26) groups were significantly increased compared with the control group (P= 0.037 vs. 0.024). Conclusion: Overexpression of miR-630 led induction of T-ALL cell growth and reduction of their apoptosis. These results emphasized that miR-630 contributed as an oncogenic microRNA in T-ALL cells