Treatment of the ovarian cancer cells with recombinant MFAP5 and subsequent immunostaining showed increased density and organization of the F-actin cytoskeleton, which was abrogated by siRNA knockdown of TNNC1. Therefore, it was proposed that TNNC1 likely functions mechanistically by facilitating the formation and reorganization of cytoskeletal F-actin to enhance traction forces that underlie motility of ovarian cancer cells. This evidence concerns the gene TNNC1 and ovarian carcinoma.