MicroRNAs (miRNAs) are small noncoding RNA, approximately 18-23 nucleotides that can post-transcriptionally regulate the expression of complementary mRNAs. MiRNAs have been found to play a critical role in a broad spectrum of biological processes, such as developmental timing, cell death, cell proliferation, hematopoiesis, and nervous system patterning. Here, we aimed to investigate the possible upregulation of miR-141 in cervical cancer cells and to confirm the influential role of miR-141 in cervical cancer cell proliferation. The level of miR-141 in HeLa cells has been assessed using quantitative real-time PCR (qRT-PCR). Cell morphology and a number of living HeLa cells were achieved upon transfection with either precursor miR-141 (pre-miR-141) or a specific inhibitor. MTT assay and lactate dehydrogenase (LDH) production were monitored to assess the potential toxic effect of miR-141 in cancer cells. ELISA assay has been used to monitor the produced cytokines from transfected HeLa cells. Notably, the expression of miR-141 significantly increased in HeLa cells compared to the normal cervical HCK1T cell line. Transfection of HeLa cells with an inhibitor, antagonist miR-141, showed a potent effect on cancer cell viability, unlike the transfection of pre-miR-141. HeLa cells transfected with pre-miR-141 showed decreased levels of interleukin 13 (IL-13). Meanwhile, the transfection of miR-141 specific inhibitor showed an increasing level of produced IL-10 and a decreasing level of IL-10, indicating the role of miR-141 in avoiding programmed cell death in HeLa cells. Together, these data uncover the role of miR-141 in supporting cervical cancer progression and provide miR-141 as a believable therapeutic target.