Membrane tension is closely related to a series of cellular events, including cell movement and morphology. Defects in these cellular events are linked to various pathological processes including neurodevelopmental disorders and tumor progression and metastasis. Therefore, development of new molecular tools that control cell movement and morphology can be expected via modulating membrane tension. However, few studies have been published on the regulation of cellular events by altering membrane tension. Here we report our approach to develop a new tool for regulating cellular events by changing membrane tension. Amphipathic regions of membrane remodeling proteins are known to insert themselves into membrane bilayers. We hypothesized that these amphipathic peptides can change membrane tension by the interaction with membrane. Several amphipathic peptides derived from membrane remodeling proteins were synthesized and the effects of these peptides on F-actin distribution were evaluated. An amphipathic peptide derived from Influenza M2 protein (M2) was thus selected which yielded a polarized actin distribution and a lamellipodia formation. FBP17 has been reported as a membrane tension sensor, involved in lamellipodia formation. The percentage of cells forming lamellipodia was reduced by FBP17 knockdown. This result suggested that lamellipodia formation by M2 was driven by FBP17. Wound healing assay was performed for investigation into influence of M2 on cell movement. Effect of M2 on neurite outgrowth from primary cultured neurons was also studied.