Objective: The development of the human placenta depends on proliferation and differentiation of trophoblastic cells. Deficiencies in trophoblastic functions are known to have a critical role in the progression of placental pathologies such as preeclampsia. Therefore, in this research, it was aimed to evaluate the responses of trophoblastic cells to tumor necrosis factor-α (TNF-α) mediated cellular stress. Materials and Methods: In this study, the cellular stress model was set up by treating JAR cells with 100ng/ml TNF-α for 1, 6, 12 and 24 hour long periods. In this model, the effects of TNF-α on the proliferation capacity and apoptotic activity of JAR trophoblastic cells were investigated by immunocytochemistry. The nuclear and total expression levels of nuclear factor-κB (NF-κB) was evaluated with immunocytochemistry and Western blot, respectively. Results: It was shown that 100 ng/ml TNF-α treated cells had a reduced proliferative capacity and increased apoptotic activity by immunocytochemical staining of PCNA and caspase-8 proteins respectively. In this respect, the NF-κB signaling pathway plays a critical role in TNF-α induced processes. So that, it was shown that the TNF-α treated group had increased nuclear and total NF-κB expressions compared to the untreated one. Conclusion: Our findings showed that TNF-α has a significant role as a cellular stress source in JAR cells. TNF-α stimulated cellular response could be defined as decreased proliferative capacity, increased apoptotic activity and NF-κB signaling in JAR syncytiotrohoblastic cell lines. Therefore, investigation of TNF-α related cellular responses especially NF-κB signaling is further required for the understanding of the mechanism of placental pathologies which is crucial for the development of therapeutic approaches.