Malignant glioma is a clinically formidable disease. It commonly leads to death within 5 years after diagnosis. Physicians are often baffled since the inevitable diffuse invasion deteriorates clinical outcomes rapidly. Therefore, cancerous infiltration presents a foremost challenge to all therapeutic strategies on glioblastoma multiforme (GBM). Previously, we demonstrated that nicotinic acid (NA) possesses a brand new function by targeting F-actin stress fibers. By treating HEK293 or NIH3T3 cells with a certain concentration of NA, the F-actin stress fiber was significantly disassembled. This notable finding inspired us to explore NA further in cancer cell lines, such as GBM cells, since F-actin stress fibers are the critical foundation of cell migration, proliferation and numerous essential signaling pathways. Expectedly, we observed that optimized concentrations of NA, 3.5 mM and 7.0 mM, detached U251 from culturing petri dishes. Moreover, 7.0 mM of NA was capable of disrupting the leading-edge assembly. Additionally, we collected paraffin specimens from 85 GBM patients and evaluated the expression pattern of paxillin. Notably, we found that discernable paxillin signals were detected in 67 out of 85 samples. Given that leading edge is critical for cancer cell migration, we propose that NA treatment may be developed into a potential therapy for malignant glioma.